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Sample records for adhesion molecule-1 icam-1

  1. Signaling through intercellular adhesion molecule 1 (ICAM-1) in a B cell lymphoma line

    DEFF Research Database (Denmark)

    Holland, J; Owens, T

    1997-01-01

    Intercellular adhesion molecule 1 (ICAM-1) (CD54) is an adhesion molecule of the immunoglobulin superfamily. The interaction between ICAM-1 on B lymphocytes and leukocyte function-associated antigen 1 on T cells plays a major role in several aspects of the immune response, including T-dependent B...... cell activation. While it was originally believed that ICAM-1 played a purely adhesive role, recent evidence suggests that it can itself transduce biochemical signals. We demonstrate that cross-linking of ICAM-1 results in the up-regulation of class II major histocompatibility complex, and we...... investigate the biochemical mechanism for the signaling role of ICAM-1. We show that cross-linking of ICAM-1 on the B lymphoma line A20 induces an increase in tyrosine phosphorylation of several cellular proteins, including the Src family kinase p53/p56(lyn). In vitro kinase assays showed that Lyn kinase...

  2. Association of Intercellular Adhesion Molecule 1 (ICAM1) with Diabetes and Diabetic Nephropathy

    OpenAIRE

    Gu, Harvest F; Jun eMa; Gu, Karolin T.; Kerstin eBrismar

    2013-01-01

    Diabetes and diabetic nephropathy are complex diseases affected by genetic and environmental factors. Identification of the susceptibility genes and investigation of their roles may provide useful information for better understanding of the pathogenesis and for developing novel therapeutic approaches. Intercellular adhesion molecule 1 (ICAM1) is a cell surface glycoprotein expressed on endothelial cells and leukocytes in the immune system. The ICAM1 gene is located on chromosome 19p13 within ...

  3. Association of Intercellular Adhesion Molecule 1 (ICAM1 with Diabetes and Diabetic Nephropathy

    Directory of Open Access Journals (Sweden)

    Harvest F Gu

    2013-01-01

    Full Text Available Diabetes and diabetic nephropathy are complex diseases affected by genetic and environmental factors. Identification of the susceptibility genes and investigation of their roles may provide useful information for better understanding of the pathogenesis and for developing novel therapeutic approaches. Intercellular adhesion molecule 1 (ICAM1 is a cell surface glycoprotein expressed on endothelial cells and leukocytes in the immune system. The ICAM1 gene is located on chromosome 19p13 within the linkage region of diabetes. In the recent years, accumulating reports have implicated that genetic polymorphisms in the ICAM1 gene are associated with diabetes and diabetic nephropathy. Serum ICAM1 levels in diabetes patients and the icam1 gene expression in kidney tissues of diabetic animals are increased compared to the controls. Therefore, ICAM1 may play a role in the development of diabetes and diabetic nephropathy. In this review, we present genomic structure, variation and regulation of the ICAM1 gene, summarized genetic and biological studies of this gene in diabetes and diabetic nephropathy and discussed about the potential application using ICAM1 as a biomarker and target for prediction and treatment of diabetes and diabetic nephropathy.

  4. FRET based quantification and screening technology platform for the interactions of leukocyte function-associated antigen-1 (LFA-1 with intercellular adhesion molecule-1 (ICAM-1.

    Directory of Open Access Journals (Sweden)

    Sandeep Chakraborty

    Full Text Available The interaction between leukocyte function-associated antigen-1(LFA-1 and intercellular adhesion molecule-1 (ICAM-1 plays a pivotal role in cellular adhesion including the extravasation and inflammatory response of leukocytes, and also in the formation of immunological synapse. However, irregular expressions of LFA-1 or ICAM-1 or both may lead to autoimmune diseases, metastasis cancer, etc. Thus, the LFA-1/ICAM-1 interaction may serve as a potential therapeutic target for the treatment of these diseases. Here, we developed one simple 'in solution' steady state fluorescence resonance energy transfer (FRET technique to obtain the dissociation constant (Kd of the interaction between LFA-1 and ICAM-1. Moreover, we developed the assay into a screening platform to identify peptides and small molecules that inhibit the LFA-1/ICAM-1 interaction. For the FRET pair, we used Alexa Fluor 488-LFA-1 conjugate as donor and Alexa Fluor 555-human recombinant ICAM-1 (D1-D2-Fc as acceptor. From our quantitative FRET analysis, the Kd between LFA-1 and D1-D2-Fc was determined to be 17.93±1.34 nM. Both the Kd determination and screening assay were performed in a 96-well plate platform, providing the opportunity to develop it into a high-throughput assay. This is the first reported work which applies FRET based technique to determine Kd as well as classifying inhibitors of the LFA-1/ICAM-1 interaction.

  5. Soluble intercellular adhesion molecule-1 (sICAM-1) and soluble interleukin-2 receptors (sIL-2R) in scleroderma skin

    DEFF Research Database (Denmark)

    Søndergaard, Klaus; Deleuran, Mette; Heickendorff, Lene;

    1998-01-01

    In order to investigate whether soluble intercellular adhesion molecule-1 (sICAM-1) and soluble interleukin-2 receptors (sIL-2R) were present in scleroderma skin, and to compare their levels to concentrations measured in plasma and clinical parameters, we examined suction blister fluid and plasma...... from 13 patients with systemic sclerosis and 11 healthy volunteers. Suction blisters and biopsies were from the transition zone between normal skin and scleroderma, and uninvolved abdominal skin. The levels of sICAM-1 and sIL-2R were significantly increased in both plasma and suction blister fluid from...... systemic sclerosis patients compared with healthy volunteers. ICAM-1 was localized to vessels and perivascular mononuclear infiltrates by immunohistochemical methods. IL-2R was expressed by CD3-positive cells. The elevated levels of sICAM-1 and sIL-2R in suction blister fluid point towards activation...

  6. Study on the serum levels of soluble intercellular adhesion molecule-1 (sICAM-1) in patients with Helicobacter pylori Infection

    Institute of Scientific and Technical Information of China (English)

    吴勤动; 朱永良; 石益海

    2002-01-01

    Objective: To evaluate the interaction between serum levels of soluble intercellular adhesion molecule-1 (sICAM-1) and Helicobacter pylori (H. pylori) infection in patients with chronic gastritis and peptic ulcer. Methods: The serum levels of sICAM-1 in 205 patients with chronic gastric diseases were detected by ELISA method and the status of H. pylori was determined by histologic examination, RUT, 14C - UBT, and serology. The sera obtained from 18 healthy volunteers served as controls. Results: The serum levels of sICAM-1 were significantly higher in patients with H. pylori positive than those of H. pylori negative (889.43±32.52 ng/ml vs. 747.07±30.45 ng/ml, P<0.05). The serum levels of sICAM-1 in patients with mild, moderate and severe infection of H. pylori were 841.68±72.36 ng/ml, 905.43±37.59 ng/ml and 1012.54±49.34 ng/ml,respectively (P<0.05). The serum levels of sICAM-1 proved to be significantly correlated with the density of H. pylori colonization in gastric mucosa (rs =0.316, P<0.001). The serum levels of sICAM-1 in patients with chronic gastritis and peptic ulcer were significantly higher than those in healthy controls (P<0.05). Conclusions: These results indicated that H. pylori infection up-regulates the expression of sICAM-1.

  7. Lauric acid abolishes interferon-gamma (IFN-γ)-induction ofIntercellular AdhesionMolecule-1 (ICAM-1) andVascularCellAdhesionMolecule-1 (VCAM-1) expression in human macrophages

    Institute of Scientific and Technical Information of China (English)

    Wei-Siong Lim; Mary-Shi-Ying Gan; Melissa-Hui-Ling Ong; Choy-Hoong Chew

    2015-01-01

    Objective:To investigate the effect of different concentrations of lauric acid on Intercellular Adhesion Molecule-1 (ICAM-1) and Vascular Cell Adhesion Molecule-1 (VCAM-1) expression in IFN-γ stimulated human monocytic THP-1 cell line.Methods:THP-1 cell were cultured using Roswell Park Memorial Institute medium supplemented with 10% fetal bovine serum. THP-1 monocytes were firstly differentiated into macrophages by using phorbol-12-myristate-13-acetate. IFN-γ response test was perfomed and total cellular RNA was extracted using TRI Reagent®LS before q-RT-PCR was carried out. Subsequently, IFN-γ treated THP-1 macrophages were stimulated with increasing doses of lauric acid for another 24 hour, before q-RT-PCR. MTT assay was carried out to investigate the effect of lauric acid on undifferentiated and differentiated THP-1 cells.Results:The mRNA expression levels of ICAM-1 and VCAM-1 were normalized toβ-actin and relatived to the untreated cells. The expressions of ICAM-1 and VCAM-1 were significantly induced in cells treated with 10 ng/mL of IFN-γ. This showed that IFN-γ could up-regulate inflammatory process and may cause atheroma formation. Although lauric acid did not have any significant impact on undifferentiated and differentiated THP-1 cell viability, the normalized fold expressions of ICAM-1 and VCAM-1 in IFN-γ-treated THP-1 macrophages were decreased significantly in a dose dependent manner with the presence of increasing doses of lauric acid.Conclusions:This study successfully proved that lauric acid was able to antagonize the up-regulatory effect of IFN-γ on ICAM-1 and VCAM-1 expressions in THP-1 macrophages. This indicates that lauric acid may be an anti-inflammatory therapeutic and prophylaxis agent for atherosclerosis.

  8. Circulating intercellular adhesion molecule-1 (ICAM-1) as an early and sensitive marker for virus-induced T cell activation

    DEFF Research Database (Denmark)

    Christensen, Jan Pravsgaard; Johansen, J; Marker, O;

    1995-01-01

    The effect of systemic virus infection on the level of circulating ICAM-1 (cICAM-1) in serum, and the role of virus-activated T cells in this context, were studied using the murine lymphocytic choriomeningitis virus infection as primary model system. A marked virus-induced elevation in cICAM-1...... in serum was revealed, the presence of which coincided with the phase of virus-induced T cell activation. However, high levels of cICAM-1 in serum were observed well before maximal T cell activation could be demonstrated. No increase in cICAM-1 was observed in the serum of infected T cell-deficient nude...... induce shedding of ICAM-1 into the circulation, and this parameter may be used as an early and sensitive marker for immune activation....

  9. The influence of propofol on the expression of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) in reoxygenated human umbilical vein endothelial cells.

    LENUS (Irish Health Repository)

    Corcoran, T B

    2012-02-03

    BACKGROUND: Leucocytes are a pivotal component of the inflammatory cascade that results in tissue injury in a large group of disorders. Free radical production and endothelial activation promote leucocyte-endothelium interactions via endothelial expression of vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) which augment these processes, particularly in the setting of reperfusion injury. Propofol has antioxidant properties which may attenuate the increased expression of these molecules that is observed. METHODS: Cultured human umbilical vein endothelial cells were exposed to 20 h of hypoxia, then returned to normoxic conditions. Cells were treated with saline, Diprivan 5 microg mL(-1) or propofol 5 microg mL(-1), for 4 h after reoxygenation and were examined for ICAM-1 and VCAM-1 expression. RESULTS: Hypoxia did not increase the expression of ICAM-1\\/VCAM-1. ICAM-1 expression peaked 12 h after reoxygenation (21.75(0.6) vs. 9.6(1.3), P = 0.02). Propofol, but not Diprivan, prevented this increase (8.2(2.9) vs. 21.75(0.6), P = 0.009). VCAM-1 expression peaked 24 h after reoxygenation (9.8(0.9) vs. 6.6(0.6), P = 0.03). Propofol and Diprivan prevented this increase, with no difference between the two treatments observed (4.3(0.3) and 6.4(0.5) vs. 9.8(0.9), P = 0.001, 0.02, respectively). CONCLUSION: These effects are likely to be attributable to the antioxidant properties of propofol, and suggest that propofol may have a protective role in disorders where free radical mediated injury promotes leucocyte-endothelium adhesive interactions.

  10. 平阳霉素作用静脉畸形内皮细胞后VCAM-1、ICAM-1、ICAM-3表达%Pingyangmycin- Regulated Expression of Vascular Cell Adhesion Molecule - 1 ( VCAM - 1 ), Intercellular Adhesion Molecule-1 (ICAM - 1 ) and Intercellular Adhesion Molecule-3 (ICAM-3) in Human Venous Malformation Endothelial Cells

    Institute of Scientific and Technical Information of China (English)

    贾玉林; 张文峰; 贾俊; 赵怡芳

    2012-01-01

    Objective: To investigate PYM-regulated expressions of VCAM-1, ICAM-1 and ICAM -3 in primary cultured HVMECs. Methods: Expressions of the adhesion molecules VCAM-1, ICAM-1 and ICAM-3 were studied in PYM -regulated HVMECs in vitro by means of ELISA and RT - PCR. Results: Expressions of VCAM-1 and ICAM -3 were induced, and expression of ICAM-1 was up-regulated, both in a time and concentration-dependent fashion after stimulation with PYM. The expression of VCAM - 1 was observed at 2h and ICAM-1 at 6h and ICAM-3 at 12h. The highest expression of VCAM-1, ICAM-1 and ICAM-3 was observed at 8h, 18h and 24h, After exposed for the same time interval, expression of adhesion molecules on HVMECs exposed to lmg/L of PYM was higher than that exposed to other concentration of PYM. mRNA expressions of VCAM-1, ICAM-1 and ICAM -3 started at 2h, 6h and 12h respectively. Maximal synthetic activity was observed at 6 - 8h for VCAM-1, at 12-18h for ICAM-1 and at 18 -24h for ICAM -3. Synthesis activity was greatly suppressed at l0mg/L or higher concentration. Conclusion: Expression of Ig-like adhesion molecules in HVMECs can be induced or up-regulated by lower concentration of PYM in a time and concentration -dependent fashion.%目的:研究平阳霉素(PYM)作用于人静脉畸形内皮细胞(HVMECs)后Ig粘附分子(VCAM-1、ICAM-1、ICAM-3)表达.方法:体外培养HVMECs,采用细胞ELISA和RT- PCR技术检测不同浓度PYM作用人HVMECs后Ig粘附分子表达.结果:PYM作用人HVMECs后粘附分子表达具有时间浓度效应.PYM能诱导VCAM-1在人HVMECs表达,2h后明显增高,8h后达到峰值,12h后下降,48 h后呈阴性表达.PYM能促进ICAM-1在人HVMECs表达,12h后显著增高,18 h最高,24 h逐渐下降.PYM能促进ICAM-3表达,12 h后逐渐增高,24 h达到峰值,72 h后1CAM-3仍高表达.0.01~1 mg/L PYM能诱导或促进粘附分子表达,表达水平与药物浓度成正相关,1 mg/L PYM作用人HVMECs后粘附分子表达较高,10 mg/L PYM

  11. Transfected HEK293 Cells Expressing Functional Recombinant Intercellular Adhesion Molecule 1 (ICAM-1) - A Receptor Associated with Severe Plasmodium falciparum Malaria

    DEFF Research Database (Denmark)

    Bengtsson, Anja; Joergensen, Louise; Barbati, Zachary R;

    2013-01-01

    as vaccine candidates and go into clinical trials. Such studies require availability of functional recombinant ICAM-1 in large quantities. In this study, we compared recombinant ICAM-1 expressed in HEK293 and COS-7 cells with mouse myeloma NS0 ICAM-1 purchased from a commercial vendor in terms of protein...... purity, yield, fold, ability to bind DBLβ, and relative cost. We present a HEK293 cell-based, high-yield expression and purification scheme for producing inexpensive, functional ICAM‑1. ICAM-1 expressed in HEK293 is applicable to malaria research and can also be useful in other research fields....

  12. Intercellular adhesion molecule-1 clusters during osteoclastogenesis

    NARCIS (Netherlands)

    V. Bloemen; T.J. de Vries; T. Schoenmaker; V. Everts

    2009-01-01

    Adhesion between osteoblasts and osteoclast precursors is established via an interaction involving intercellular adhesion molecule-1 (ICAM-1) on osteoblasts and leukocyte function-associated antigen-1 (LFA-1) on osteoclast precursors. The latter cells also express ICAM-1, but little is known about t

  13. Lauric acid abolishes interferon-gamma (IFN-γ-induction of intercellular adhesion molecule-1 (ICAM-1 and vascular cell adhesion molecule-1 (VCAM-1 expression in human macrophages

    Directory of Open Access Journals (Sweden)

    Wei-Siong Lim

    2015-09-01

    Conclusions: This study successfully proved that lauric acid was able to antagonize the up-regulatory effect of IFN-γ on ICAM-1 and VCAM-1 expressions in THP-1 macrophages. This indicates that lauric acid may be an anti-inflammatory therapeutic and prophylaxis agent for atherosclerosis.

  14. The immunohistochemical study of interleukin-1 to Regulate Intercellular adhesion molecule-1 expression on cultured human gingival fibroblasts and periodontal ligament fibroblasts%IL-1β对牙龈成纤维细胞和牙周膜细胞上ICAM-1表达调节的免疫组化研究

    Institute of Scientific and Technical Information of China (English)

    罗志晓; 李成章; 曹正国

    2002-01-01

    目的: 了解牙龈成纤维细胞(human gingival fibroblast,HGF)、牙周膜细胞(periodontal ligament fibroblast,PDLF)上细胞间粘附分子1(intercellular adhesion molecule-1,ICAM-1)的表达以及白细胞介素-1β(interleukin-1β,IL-1β)作用后ICAM-1的表达.方法: 取正畸拔牙,体外培养牙龈成纤维细胞和牙周膜细胞,检测其未受和受IL-1β作用后ICAM-1的表达情况,图像分析结果.结果: 正常牙龈成纤维细胞、牙周膜细胞上ICAM-1表达阴性或弱阳性,IL-1β作用后,ICAM-1表达强阳性,和对照组相比,有显著性差异(P<0.01).结论: 牙龈成纤维细胞、牙周膜细胞受IL-1β作用后ICAM-1的表达增强,提示ICAM-1参与牙周炎的病理过程.

  15. 细胞间粘附因子-1在非小细胞肺癌表达的临床意义%The clinical significance of intercellular adhesion molecule-1(ICAM-1) expression in human non small cell lung cancer

    Institute of Scientific and Technical Information of China (English)

    于晓锋; 王红卫; 李文军; 张宏伟

    2005-01-01

    目的探讨细胞间粘附因子-1(Intercellular adhesion molecule-1,ICAM-1)在肺癌组织中的表达及其与肺癌侵袭转移和预后的关系.方法回顾性分析86例非小细胞肺癌患者的手术切除标本,采用免疫组化SP法检测肺癌组织中的ICAM-1的表达,用χ2检验分析其表达与肺癌生物学行为的关系;生存分析用Kaplan-Meier生存曲线和Log-Rank检验.结果肺癌组织ICAM-1表达率为37.21%,鳞癌表达略高于腺癌;淋巴转移的肺癌组织ICAM-1表达率高于无淋巴结转移者;Ⅰ期肺癌中ICAM-1阳性率高于Ⅱ期,Ⅱ期高于Ⅲ期;术后转移组ICAM-1的阳性表达率低于无转移组;ICAM-1阳性表达患者术后转移率低于阴性患者;ICAM-1阳性表达的患者5年生存率高于ICAM-1阴性表达患者.结论非小细胞肺癌组织中ICAM-1的表达与病理类型无关;与病理分期、淋巴转移呈负相关;与术后患者血行转移和生存时间呈负相关.ICAM-1是判断非小细胞肺癌患者转移和预后的重要因素.

  16. The Relativity Study between Soluble E-selectin and Soluble Intercellular Adhesion Molecule-1 and Diabetic Retinopathy%sE-选择素和sICAM-1与糖尿病性视网膜病变的相关性研究

    Institute of Scientific and Technical Information of China (English)

    张炜; 蔡雷鸣; 张燕; 杜培宜; 谭龙益; 王梅芳; 张蓉; 孙国庆

    2015-01-01

    目的:检测糖尿病性视网膜病变患者血清中sE-选择素和sICAM-1的水平,研究sE-选择素和sICAM-1在糖尿病性视网膜病变发生、发展中的作用及其二者之间的关系。方法选择糖尿病性视网膜病变患者50例;无糖尿病性视网膜病变的2型糖尿病患者100例;年龄、性别相当的正常对照组50例。空腹抽静脉血,采用酶联免疫吸附法(ELISA法)对sE-选择素和sICAM-1进行检测,比较各组之间统计学差异以及sE-选择素和sICAM-1之间的相关性。结果糖尿病性视网膜病变组(A组)和无糖尿病性视网膜病变组(B组)sE-选择素和sICAM-1与对照组(C组)比较均有显著性差异(P<0.01);糖尿病性视网膜病变组(A组)与无糖尿病性视网膜病变组(B组)比较,差异有显著性意义(P<0.01)。糖尿病性视网膜病变组中sE-选择素和sICAM-1呈正相关(r=0.836,P<0.001)。结论 sE-选择素和sICAM-1的测定或许有助于糖尿病性视网膜病变的早期诊断,可能对糖尿病视网膜病变发生和发展有提示意义。%ObjectiveTo observe the level of serum soluble E-selectin (sE-selectin) and soluble intercellular adhesion molecule-1(sICAM-1) in diabetic retinopathy patients, and to detect the relationship between the sE-selectin and sICAM-1 and the diabetic retinopathy.MethodsThe serum levels of E-selectin (sE-selectin) and intercellular adhesion molecule-1(sICAM-1) were measured respectively in diabetic retinopathy patients and diabetic patients without diabetic retinopathy as well as normal people. The data were analyzed between the three groups.ResultsThe level of sE-selectin and sICAM-1 in normal group were signiifcantly lower than the diabetic retinopathy patients and diabetic patients without diabetic retinopathy (P<0.01). The level of sE-selectin and sICAM-1 in diabetic retinopathy patients were signiifcantly higher than the diabetic patients without diabetic

  17. 脑梗死伴牙周炎患者CRP、 IL-6和sICAM-1水平检测的研究%Clinical significance of C-reactive protein, interleukin-6 and soluble intercellular adhesion molecule 1 in patients with cerebral infarction and periodontal disease

    Institute of Scientific and Technical Information of China (English)

    裴路; 曹潇方; 张瑞敏; 付锦

    2011-01-01

    Objective: To explore the possible relationship of serum levels of C-reactive protein ( CRP), interleukin-6 (IL-6) and soluble intercellular adhesion molecule 1 ( sICAM- 1 ) of patients with chronic periodontitis (CP) and cerebral infarction (CI).Methods: 133 subjects were included in this study.Among them, 33 were patients with CI and CP (group CI + CP), 30 with CP (group CP), 32 with CI (group CI) and 38 were healthy volunteers (group H).The periodontal indexes and the serum levels of CRP, IL-6 and sICAM-1 were measured.Results: The periodontal indexes including calculus index, bleeding on probing, probing depth and attachment loss were significantly different among the four groups.In groups of CI + CP, CP and Cl the CRP, IL-6 and sICAM-1 levels were significantly higher than those in the group H(P <0.01 ).Conclusion: CRP, IL-6 and sICAM-1 might be closely related with the pathogenesis of CI and CP.A certain correlation might exist between CI and CP.%目的:探讨慢性牙周炎与脑梗死患者血清中C- 反应蛋白(CRP)、白细胞介素6(IL- 6)和可溶性细胞间黏附分子1(sICAM- 1)水平变化及相关关系.方法:纳入经头颅CT或MRI证实确诊脑梗死并伴牙周炎的患者[(CI+CP)组]33例,单纯慢性牙周炎患者(CP组)30例,脑梗死患者(CI组)32例和健康志愿者(H组)38例.记录简化牙石指数、探诊岀血阳性率、探诊深度和附着水平丧失,检测血清中CRP、IL- 6和sICAM- 1的含量.结果:各组间牙周病指数差异有显著性(P<0.05),与CP组、CI组、H组相比,(CI+CP)组的CRP、IL- 6和sICAM- 1水平明显升高(P<0.01).结论:CRP、IL- 6和sICAM- 1可能与脑梗死和牙周炎病理机制相关,牙周炎和脑梗死之间存在一定的关联.

  18. 构建人ICAM-1真核表达载体的实验研究%CONSTRUCTION AND EXPRESSION OF HUMAN INTERCELLULAR ADHESION MOLECULE- 1 EXPRESSION VECTOR

    Institute of Scientific and Technical Information of China (English)

    陈志鸿; 静雅杰; 宋宝辉

    2007-01-01

    目的:构建人ICAM-1-1真核表达载体pcDNA3.1(-)-ICAM-1.方法:设计特异性引物,利用PCR技术扩增出ICAM-1全编码区基因片段,插入到真核表达载体pcDNA3.1(-)中.结果:PCR扩增得到人成熟ICAM-1的cDNA片段大小为1800bp,重组子利用限制性内切酶进行酶切鉴定和DNA序列分析得到真核表达载体pCDA3.1(-)-ICAM-1.结论:成功构建了人ICAM-1真核表达载体,为进一步建立稳定转染ICAM-1的细胞株以及研究ICAM-1及其受体的生物学功能提供了条件.

  19. Angiogenic Effect of Intercellular Adhesion Molecule-1

    Institute of Scientific and Technical Information of China (English)

    DENG Chenguo; ZHANG Duanlian; SHAN Shengguo; WU Jingwen; YANG Hong; YU Ying

    2007-01-01

    In order to investigate the angiogenic effect of intercellular adhesion molecule-1 (ICAM-1), two parts of experiment were performed. Chick embryo chorioallantoic membrane (CAM) assay was used for in vivo angiogenic research. The chick embryos were divided into 4 groups: ICAM-1 group (divided into 3 subgroups, Ⅰ, Ⅱ and Ⅲ) for screening the angiogenic effect of ICAM-1 by adding different concentrations of ICAM-1 (0.1, 0.2 and 0.3 μg/μL) 5 μL into the chick embryo CAMs on the day 10 after incubation for every subgroup; Anti-ICAM-1 group A (divided into 2 subgroups, Ⅰ and Ⅱ) by adding different concentrations of Anti-ICAM-1 (1:100, 1:50) 5 μL into the chick embryo CAMs on the day 10 after incubation for every subgroup to evaluate the effect of ICAM-1 on the survival of microvessels through observing whether Anti-ICAM-1 could induce involution of the microvessels on CAMs; Anti-ICAM-1 group B (divided into 2 subgroups, Ⅰ and Ⅱ ) by adding different concentrations of Anti-ICAM-1 (1:100, 1:50) 5 μL into the chick embryo CAMs on the day 6 after incubation for every subgroup to evaluate whether ICAM-1 involved in embryonic angiogenesis through observing the growth of microvessels on CAMs; Control group: ICAM-1 or Anti-ICAM-1 was substituted by PBS 5 μL on the day 10 or day 6 after incubation. Three days later, the CAMs were photographed in vivo, excised, sectioned and the number of microvessels was counted. In ICAM-1 group, there was increased number of microvessels arranged radially with "spoked-wheel" pattern around the gelatin sponges. The new microvessels growing perpendicularly to gelatin sponges were observed. The number of the microvessels growing in the CAM mesenchymes around the sponges in 3 subgroups was higher than that in control group (P<0.01), however, there was no significant difference among the 3 subgroups (P>0.05). In anti-ICAM-1 group A, the radially arranged microvessels were very unclear around the sponges contrast to that of ICAM

  20. Blockage of intercellular adhesion molecule-1 (ICAM-1 in the prevention of reperfusion lesion in the skeletal musculature of EPM-1 Wistar rats Bloqueio das moléculas de adesão intercelular-1 (ICAM-1 na prevenção da lesão de reperfusão na musculatura esquelética de ratos Wistar EPM-1

    Directory of Open Access Journals (Sweden)

    Roberto David Filho

    2004-12-01

    Full Text Available Purpose: Ischemia-reperfusion lesions are a form of acute inflammation in which leukocytes are considered to play a pivotal role. This study was made with the objective of determining whether the blockage of intracellular adhesion molecule-1, involved in the diapedesis of leukocytes, is efficacious in minimizing this lesions in the skeletal musculature of the posterior limbs of rats. Methods: The juxta-infrarenal aorta of three groups of six adult rats was clipped for six hours. After this, one group was sacrificed (control group and the others underwent 24 hours of reperfusion, one with 0.9% physiological saline (reperfusion group and the other with anti-ICAM-1 monoclonal antibodies (ICAM-1 group. A myeloperoxidase assay was utilized for estimating the infiltrate of neutrophils. Biopsies were obtained to make thin sections of hematoxylin-eosin and NADH. Blood samples were collected for making assays of biochemical parameters (creatinine; potassium; DHL; leukogram; venous pH; CK. Results: The myeloperoxidase levels were raised in the reperfusion (p Objetivo: As lesões de isquemia-reperfusão (I/R são uma forma de inflamação aguda na qual os leucócitos são considerados como tendo um papel fundamental. Este estudo foi feito com o objetivo de determinar se o bloqueio das Moléculas de Adesão Intercelular -1 (ICAM-1, envolvidas na diapedese dos leucócitos, é eficaz em minimizar estas lesões na musculatura esquelética dos membros posteriores de ratos. Métodos: A aorta infra-renal de três grupos de seis ratos adultos foi clampeada por seis horas. Logo após, um grupo foi sacrificado (grupo controle e os outros foram submetidos a 24 horas de reperfusão, um com solução salina fisiológica 0,9% (grupo reperfusão e outro com anticorpos monoclonais anti-ICAM-1 (grupo ICAM-1. A quantificação da enzima mieloperoxidase foi utilizada para estimar o infiltrado de leucócitos na musculatura. Biópsias foram obtidas e coradas com hematoxilina

  1. ICAM-1-activated Src and eNOS signaling increase endothelial cell surface PECAM-1 adhesivity and neutrophil transmigration.

    Science.gov (United States)

    Liu, Guoquan; Place, Aaron T; Chen, Zhenlong; Brovkovych, Viktor M; Vogel, Stephen M; Muller, William A; Skidgel, Randal A; Malik, Asrar B; Minshall, Richard D

    2012-08-30

    Polymorphonuclear neutrophil (PMN) extravasation requires selectin-mediated tethering, intercellular adhesion molecule-1 (ICAM-1)-dependent firm adhesion, and platelet/endothelial cell adhesion molecule 1 (PECAM-1)-mediated transendothelial migration. An important unanswered question is whether ICAM-1-activated signaling contributes to PMN transmigration mediated by PECAM-1. We tested this concept and the roles of endothelial nitric oxide synthase (eNOS) and Src activated by PMN ligation of ICAM-1 in mediating PECAM-1-dependent PMN transmigration. We observed that lung PMN infiltration in vivo induced in carrageenan-injected WT mice was significantly reduced in ICAM-1(-/-) and eNOS(-/-) mice. Crosslinking WT mouse ICAM-1 expressed in human endothelial cells (ECs), but not the phospho-defective Tyr(518)Phe ICAM-1 mutant, induced SHP-2-dependent Src Tyr530 dephosphorylation that resulted in Src activation. ICAM-1 activation also stimulated phosphorylation of Akt (p-Ser473) and eNOS (p-Ser1177), thereby increasing NO production. PMN migration across EC monolayers was abolished in cells expressing the Tyr(518)Phe ICAM-1 mutant or by pretreatment with either the Src inhibitor PP2 or eNOS inhibitor L-NAME. Importantly, phospho-ICAM-1 induction of Src signaling induced PECAM-1 Tyr686 phosphorylation and increased EC surface anti-PECAM-1 mAb-binding activity. These results collectively show that ICAM-1-activated Src and eNOS signaling sequentially induce PECAM-1-mediated PMN transendothelial migration. Both Src and eNOS inhibition may be important therapeutic targets to prevent or limit vascular inflammation. PMID:22806890

  2. Intercellular adhesion molecule-1 in patients with idiopathic interstitial pneumonia.

    Directory of Open Access Journals (Sweden)

    Takehara H

    2001-08-01

    Full Text Available This study focuses on a possible role of intercellular adhesion molecule-1 (ICAM-1 in interstitial pulmonary diseases. We determined a soluble form of ICAM-1 in serum and bronchoalveolar lavage fluid (BALF using ELISA in patients with usual interstitial pneumonia (UIP, bronchiolitis obliterance organizing pneumonia (BOOP, or nonspecific interstitial pneumonia (NSIP. In addition, we investigated the expression of ICAM-1 in the lung tissues of these patients by means of immunohistochemical staining. Serum levels of soluble ICAM-1 were significantly higher in patients with UIP or NSIP than in healthy subjects, and were also high in patients with BOOP. The soluble ICAM-1 in BALF tended to be higher in patients with UIP, BOOP, or NSIP than in normal subjects. A significant correlation was seen between soluble levels of ICAM-1 in serum and BALF. In the immunostaining of ICAM-1 of the lung tissues, ICAM-1 expression was more pronounced in patients with UIP than in those with BOOP or NSIP. The increased expression of ICAM-1 was seen in type II alveolar epithelium and vascular endothelium in patients with interstitial pneumonia. A positive correlation was observed between the degree of ICAM-1 expression in the lung tissues and the BALF levels of soluble ICAM-1. The expression of ICAM-1 in type II alveolar epithelium suggests that ICAM-1 plays a specific role in the fibrotic process of the lung, and that the measurement of soluble ICAM-1 in sera and BALF could be a useful marker for evaluating the progression of fibrosis.

  3. Effects of peroxisome proliferator-activated receptors-γagonist on erythrocyte aggregation and serum soluble intercellular adhesion molecules-1 in patients with impaired glucose regulation%PPAR-γ激动剂对糖调节受损患者红细胞聚集性及血清sICAM-1的影响

    Institute of Scientific and Technical Information of China (English)

    刘璠; 董闪闪; 周慧敏; 郭玉卿

    2014-01-01

    目的:观察过氧化物酶体增殖物激活受体-γ( PPAR -γ)激动剂罗格列酮对糖调节受损( IGR)患者红细胞聚集性的影响,并探讨其作用机制。方法选取IGR患者90例,按随机数字表方法随机分为对照组45例和实验组45例。对照组给予生活方式干预,实验组给予生活方式联合罗格列酮4 mg/d 干预,疗程6个月。治疗前及治疗后第3,6个月测糖化血红蛋白( HbA1 c)、红细胞聚集指数( EAI)、血清可溶性细胞间黏附分子-1( sICAM -1)。结果治疗前2组HbA1C、sICAM -1及EAI均无显著性差异(P均>0.05);治疗后2组HbA1 c、EAI及血清 sICAM -1均显著下降(P 均<0.01);且实验组 HbA1 c、EAI 及血清 sI-CAM -1显著低于对照组(P均<0.01);治疗后6个月实验组 EAI 和血清 sICAM -1与3个月时比较均显著降低(P均<0.01),2组HbA1 c及对照组EAI、血清sICAM -1与3个月时比较无显著性差异(P均>0.05);sICAM -1与 EAI和 HbA1C均呈正相关(P<0.05和0.01)。结论 PPAR -γ激动剂可通过降低 IGR 患者血清 sICAM -1水平,改善其红细胞集聚性,预防糖尿病血管并发症的发生、发展。%Objective It is to observe the influence of peroxisome proliferator-activated receptors-γ( PPAR-γ)agonist rosiglitazone on erythrocyte aggregation in patients with impaired glucose regulation( IGR)in order to explore its mechanism. Methods 90 patients with IGR were randomly divided into control group(n=45)and experimental group(n=45). The pa-tients were treated with lifestyle interventions in control group while lifestyle interventions combined with rosiglitazone(4 mg/d)in experimental group for 6 months. Hemoglobin A1c(HbA1c),erythrocyte aggregation index(EAI)and serum soluble intercellular adhesion molecules-1(sICAM -1)were measured before and 3,6 months after treatment. Results Before treat-ment,there were no significant difference between two groups in HbA1c

  4. Levels of soluble cell adhesion molecules- 1 and interferon- γ in plasma of patients with coronary heart disease%冠心病患者血浆sICAM-1和IFN-γ的水平

    Institute of Scientific and Technical Information of China (English)

    石胜伟; 李清贤; 王雪楠; 郭焕

    2007-01-01

    目的 探讨可溶性细胞黏附因子-1(sICAM-1)和γ干扰素(IFN-γ)在冠心病发病过程中的作用及其临床意义.方法 采用酶联免疫吸附试验法(ELISA)对50例冠心病人(急性心梗14例,不稳定心绞痛16例,稳定性心绞痛20例)和30例正常人血浆中sICAM-1和IFN-γ水平进行检测. 结果冠心病患者血浆sICAM-1和IFN-γ的水平分别为(344.25±70.55)ng/ml和(1.877±0.104)pg/ml,显著高于正常对照组(146.35±32.69)ng/ml和(0.072±0.014)pg/ml(P<0.05);急性心梗组二者的水平分别为(453.54±83.92)ng/ml和(2.316±0.129)pg/ml,显著高于不稳定型心绞痛组[(309.96±55.74)ng/ml和(1.722±0.047)pg/ml]和稳定型心绞痛组[(244.37±60.23)ng/ml和(1.223±0.132)pg/ml](P<0.05).结论 血浆sCAM-1和IFN-γ与冠心病的发生与发展相关,二者水平的检测对冠心病诊断及病情监测有重要意义.

  5. Effects of irradiation on the expression of the adhesion molecules (NCAM, ICAM-1) by glioma cell lines

    Energy Technology Data Exchange (ETDEWEB)

    Yamanaka, Ryuya; Tanaka, Ryuichi; Yoshida, Seiichi (Niigata Univ. (Japan). Brain Research Inst.)

    1993-11-01

    The expression of the intercellular adhesion molecule-1 (ICAM-1) and neural cell adhesion molecule (NCAM) by glioma cell lines was investigated. The effects of interferon (IFN)-[gamma] or irradiation on the expression was also assessed. Two glioma cell lines showed more than 75% NCAM-positive cells. After treatment with IFN-[gamma] or irradiation, another three cell lines were induced to show more than 50% positive cells. Three glioma cell lines showed more than 50% ICAM-1-positive cells. After treatment with IFN-[gamma], another two cell lines were induced to show more than 50% positive cells. After treatment with irradiation, one more cell line was induced to show more than 50% positive cells. ICAM-1 and NCAM expression by glioma cell lines is susceptible to modulation by IFN-[gamma] or irradiation. (author).

  6. Engagement of PSGL-1 enhances β2-integrin-involved adhesion of neutrophils to recombinant ICAM-1

    Institute of Scientific and Technical Information of China (English)

    Xiao-guang WANG; Yan-ping CHENG; Xue-qing BA

    2006-01-01

    Aim: The interactions of selectins and their ligands initiate the process of leukocyte migrating into inflamed tissue. P-selectin glycoprotein ligand 1 (PSGL-1) is the best characterized ligand of selectins, and has been demonstrated to mediate the adhesion of leukocytes to all three selectins in vivo. PSGL-1 not only functions as an anchor molecule to capture the leukocytes to the activated endothelial cells by its interaction with selectins, but also transduces the signals to activate leukocytes. Our present work aimed to investigate the mechanism by which PSGL-1-mediated signal activates neutrophils and enhances the adhesion to the endothelial cells. Methods: We detected the effects of the engagement of PSGL-1 with monoclonal antibodies (mAb) or P-selectin on the adhesion of neutrophils to the recombinant intercellular adhesion molecule-1 (ICAM-1), and on the expression of β2-integrin. Additionally, the role of cytoskeleton in these process was studied by using inhibitor cytochalasin B. Results: The engagement of PSGL-1 increased the expression of β2-integrin on the surface of neutrophils and enhanced the adhesion of neutrophils to the recombinant ICAM-1. mAb against CD 18 impaired the adhesion of PSGL-1 -engaged neutrophils to ICAM-1. Moreover, the inhibitor cytochalasin B largely blocked the increase of CD 18 expression as well as the adhesion of PSGL-1-engaged neutrophils to ICAM-1. Conclusion: The PSGL-1-transduced signals can enhance β2-integrin-involved adhesion of neutrophils to the recombinant ICAM-1, and this process depends on the dynamics of cytoskeleton.

  7. Intercellular adhesion molecule-1 expression by skeletal muscle cells augments myogenesis

    Energy Technology Data Exchange (ETDEWEB)

    Goh, Qingnian; Dearth, Christopher L.; Corbett, Jacob T. [Department of Kinesiology, The University of Toledo, Toledo, OH (United States); Pierre, Philippe [Centre d’Immunologie de Marseille-Luminy U2M, Aix-Marseille Université, Marseille (France); INSERM U631, Institut National de la Santé et Recherche Médicale, Marseille (France); CNRS UMR6102, Centre National de la Recherche Scientifique, Marseille (France); Chadee, Deborah N. [Department of Biological Sciences, The University of Toledo, Toledo, OH (United States); Pizza, Francis X., E-mail: Francis.Pizza@utoledo.edu [Department of Kinesiology, The University of Toledo, Toledo, OH (United States)

    2015-02-15

    We previously demonstrated that the expression of intercellular adhesion molecule-1 (ICAM-1) by skeletal muscle cells after muscle overload contributes to ensuing regenerative and hypertrophic processes in skeletal muscle. The objective of the present study is to reveal mechanisms through which skeletal muscle cell expression of ICAM-1 augments regenerative and hypertrophic processes of myogenesis. This was accomplished by genetically engineering C2C12 myoblasts to stably express ICAM-1, and by inhibiting the adhesive and signaling functions of ICAM-1 through the use of a neutralizing antibody or cell penetrating peptide, respectively. Expression of ICAM-1 by cultured skeletal muscle cells augmented myoblast–myoblast adhesion, myotube formation, myonuclear number, myotube alignment, myotube–myotube fusion, and myotube size without influencing the ability of myoblasts to proliferate or differentiate. ICAM-1 augmented myotube formation, myonuclear accretion, and myotube alignment through a mechanism involving adhesion-induced activation of ICAM-1 signaling, as these dependent measures were reduced via antibody and peptide inhibition of ICAM-1. The adhesive and signaling functions of ICAM-1 also facilitated myotube hypertrophy through a mechanism involving myotube–myotube fusion, protein synthesis, and Akt/p70s6k signaling. Our findings demonstrate that ICAM-1 expression by skeletal muscle cells augments myogenesis, and establish a novel mechanism through which the inflammatory response facilitates growth processes in skeletal muscle. - Highlights: • We examined mechanisms through which skeletal muscle cell expression of ICAM-1 facilitates events of in vitro myogenesis. • Expression of ICAM-1 by cultured myoblasts did not influence their ability to proliferate or differentiate. • Skeletal muscle cell expression of ICAM-1 augmented myoblast fusion, myotube alignment, myotube–myotube fusion, and myotube size. • ICAM-1 augmented myogenic processes through

  8. Increased Expression of Intercellular Adhesion Molecule-1, Vascular Cellular Adhesion Molecule-1 and Leukocyte Common Antigen in Diabetic Rat Retina

    Institute of Scientific and Technical Information of China (English)

    Ningyan Bai; Shibo Tang; Jing Ma; Yan Luo; Shaofeng Lin

    2003-01-01

    Purpose: To understand the expression and distribution of intercellular adhesion molecule- 1(ICAM- 1),vascular cellular adhesion molecule- 1 (VCAM- 1)and CD45 (Leukocyte Common Antigen) in the control nondiabetic and various courses of diabetic rats retina. To explore the role of adhesion molecules (Ams) and the adhesion of leukocytes to vascular endothelial cells via Ams in diabetic retinopathy(DR).Methods: Sixty healthy adult male Wistar rats were randomly divided into diabetic groups(induced by Streptozotocin, STZ) and normal control groups. Rats in these two groups were further randomly divided into 3, 7, 14, 30, 90 and 180 days-group,including 5 rats respectively. The immunohistochemical studies of ICAM-1, VCAM-1 and CD45 were carried out in the retinal digest preparations or retinal paraffin sections, and the results were analyzed qualitatively, semi-quantitatively.Results: No positive reaction of VCAM-1 was found, and weak reactions of ICAM-1,CD45 were found in nondiabetic rats retina. The difference of 6 control groups had no statistical significance(P > 0.05). The increased ICAM-1 and CD45 staining pattern were detectable 3 days after diabetes induction, and a few VCAM-1 positive cells were observed in the retinal blood capillaries. The difference of diabetes and control is significant( P < 0.05).Following the course, the expressions of ICAM-1, VCAM-1 and CD45 were increasingly enhanced, reaching a peak at the 14th day.Conclusion: Increased expression of ICAM-1, VCAM-1 and leukocytes adhering and stacking in retinal capillaries are the very early events in DR. Coherence of expression and distribution of the three further accounts for it is the key point for the onset of DR that Ams mediates leukocytes adhesion and endothelial cell injury.

  9. Soluble intercellular adhesion molecule-1 for stable and acute phases of idiopathic pulmonary fibrosis

    OpenAIRE

    Okuda, Ryo; Matsushima, Hidekazu; Aoshiba, Kazutetsu; Oba, Tomohiro; Kawabe, Rie; Honda, Koujiro; Amano, Masako

    2015-01-01

    The levels of soluble intercellular adhesion molecule-1 (sICAM-1) have been reported to increase in patients with idiopathic pulmonary fibrosis. However, the utility of sICAM-1 has not been reported in detail. The aim of this study was to investigate whether sICAM-1 was a useful biomarker for stable idiopathic pulmonary fibrosis (IPF) and early phase of acute exacerbation of IPF. The patients who were diagnosed with IPF between 2013 and 2015 were enrolled. The levels of sICAM-1 and other inte...

  10. Intercellular Adhesion Molecule 1 Promotes HIV-1 Attachment but Not Fusion to Target Cells

    OpenAIRE

    Naoyuki Kondo; Melikyan, Gregory B.

    2012-01-01

    Incorporation of intercellular adhesion molecule 1 (ICAM-1) into HIV-1 particles is known to markedly enhance the virus binding and infection of cells expressing lymphocyte function-associated antigen-1 (LFA-1). At the same time, ICAM-1 has been reported to exert a less pronounced effect on HIV-1 fusion with lymphoid cells. Here we examined the role of ICAM-1/LFA-1 interactions in productive HIV-1 entry into lymphoid cells using a direct virus-cell fusion assay. ICAM-1 promoted HIV-1 attachme...

  11. Inhibitors of 5-lipoxygenase inhibit expression of intercellular adhesion molecule-1 in human melanoma cells

    Institute of Scientific and Technical Information of China (English)

    Yin WANG; Bin ZHOU; Ji LI; Yong-bing CAO; Xin-sheng CHEN; Ming-he CHENG; Ming YIN

    2004-01-01

    AIM: To study the effect of 5-lipoxygenase inhibitors on the expression of intercellular adhesion molecule-1 (ICAM-1) in melanoma cells. METHODS: ICAM-1 protein of human melanoma cell a375 was detected by enzyme-linked immunosorbent, flow cytometry and Western blot analysis. Level of ICAM-1 mRNA in a375 was evaluated by Northern blot analysis. Adhesion of a375 to endothelial cell EC304 was analyzed by isotopic tracing. RESULTS:5-Lipoxygenase inhibitors nordihydroguaiaretic acid, AA861 and MK886, could suppress the expression of ICAM-1 protein as well as of its mRNA in a375 cells and reduce the adhesion of a375 to EC304. CONCLUSION:5-Lipoxygenase inhibitors can inhibit the expression of ICAM-1 in human melanoma cells and may be valuable for treatment of melanoma metastasis.

  12. Murine MicroRNA-214 regulates intracellular adhesion molecule (ICAM1) gene expression in genital Chlamydia muridarum infection

    Science.gov (United States)

    Arkatkar, Tanvi; Gupta, Rishein; Li, Weidang; Yu, Jieh-Juen; Wali, Shradha; Neal Guentzel, M; Chambers, James P; Christenson, Lane K; Arulanandam, Bernard P

    2015-01-01

    The hallmark of chlamydial infection is the development of upper genital pathology in the form of hydrosalpinx and oviduct and/or tubal dilatation. Although molecular events leading to genital tissue presentation and cellular architectural remodelling are unclear, early-stage host immune responses are believed to contribute to these long-term sequelae. Recently, we reported the contribution of selected infection-associated microRNAs (miRs) in the generation of host immunity at early-stage infection (day 6 after intravaginal Chlamydia muridarum challenge in C57BL/6 mice). In this report, we describe the contribution of an infection-associated microRNA, i.e. miR-214, to host immunity. Chlamydia muridarum infection in the C57BL/6 mouse genital tract significantly down-regulated miR-214 while up-regulating intracellular adhesion molecule 1 (ICAM1) gene expression. These in vivo observations were confirmed by establishing direct regulation of ICAM-1 by miR-214 in ex vivo genital cell cultures in the presence of miR-214 mimic and inhibitor. Because, ICAM-1 contributes to recruitment of neutrophils following infection, we also demonstrated that alteration of ICAM1 by miR-214 in interleukin-17A-deficient (IL-17A−/−) mice correlated with reduction of neutrophils infiltrating genital tissue at day 6 after challenge. Additionally, these early-stage events resulted in significantly decreased genital pathology in IL-17A−/− mice compared with C57BL/6 mice. This report provides evidence for early-stage regulation of ICAM1 by microRNAs, resulting in reduction of genital pathology associated with chlamydial infection. PMID:25865776

  13. Molecular architecture of a complex between an adhesion protein from the malaria parasite and intracellular adhesion molecule 1

    DEFF Research Database (Denmark)

    Brown, Alan; Turner, Louise; Christoffersen, Stig;

    2013-01-01

    , intercellular adhesion molecule-1 (ICAM-1). We show through small angle x-ray scattering that IT4VAR13 is rigid, elongated, and monomeric. We also show that it interacts with ICAM-1 through the DBLß domain alone, forming a 1:1 complex. These studies provide a first low resolution structural view of a PfEMP1...... ectodomain in complex with its ligand. They show that it combines a modular domain arrangement consisting of individual ligand binding domains, with a defined higher order architecture that exposes the ICAM-1 binding surface to allow adhesion....

  14. Correlation of Serum Concentrations of Soluble Thrombomodulin, Soluble Vascular Cell Adhesion Molecule-1,Intracellular Adhesion Molecule -1 And E-Selectin In Patients WithSystemic Lupus Erythematosus

    OpenAIRE

    Malak., A. Mohsen*, Magda.A.Gamil*,Maha. I.Shehata

    2003-01-01

    To date no specific serological parameters are available to assess disease activity in systemic lupus erythematosus (SLE). The objective of this study was to correlate serum levels of thrombomodulin (TM), intracellular adhesion molecule-1 sICAM-1, vascular cell adhesion molecule-1 sVCAM-1, and E-selectin with standard laboratory tests and clinical indices of disease activity in 40 patients with SLE and 20 apparently healthy persons as controls. According to British Isles Lupus Assessment Grou...

  15. Osteocyte apoptosis regulates osteoclast precursor adhesion via osteocytic IL-6 secretion and endothelial ICAM-1 expression.

    Science.gov (United States)

    Cheung, Wing-Yee; Simmons, Craig A; You, Lidan

    2012-01-01

    Osteocyte apoptosis precedes osteoclast resorption, and may act as a critical signal to trigger bone remodeling. While osteoclast precursors are known to travel via the circulation, the specific mechanisms by which they accumulate at remodeling sites are unclear. We hypothesized that osteocyte apoptosis mediates osteoclast precursor adhesion to vascular endothelium by regulating osteocytic secretion of IL-6 and soluble IL-6 receptor (sIL-6R) to promote endothelial ICAM-1 expression. We found that conditioned media from TNF-α-induced apoptotic MLO-Y4 osteocytes promoted RAW264.7 osteoclast precursor adhesion onto D4T endothelial cells (P<0.05). Blocking osteocyte apoptosis with a pan-caspase inhibitor (ZVAD-FMK) reduced osteoclast precursor adhesion to baseline levels (P<0.001). Endothelial cells treated with apoptotic osteocyte conditioned media had elevated surface expression of ICAM-1 (P<0.05), and blocking ICAM-1 abolished apoptosis-induced osteoclast precursor adhesion. Apoptotic osteocyte conditioned media contained more IL-6 (P<0.05) and sIL-6R (P<0.05) than non-apoptotic osteocyte conditioned media. When added exogenously, both IL-6 and sIL-6R were required for endothelial activation, and blocking IL-6 reduced apoptosis-induced osteoclast precursor adhesion to baseline levels (P<0.05). Therefore, we conclude that osteocyte apoptosis can promote osteoclast precursor adhesion to endothelial cells via ICAM-1; this is likely through increased osteocytic IL-6 and sIL-6R secretion, both of which are indispensible to endothelial activation. PMID:21986000

  16. Soluble intercellular adhesion molecule-1 as an early detection marker for radiation pneumonitis

    Energy Technology Data Exchange (ETDEWEB)

    Ishii, Y.; Kitamura, S. [Jichi Medical School, Dept. of Pulmonary Medicine, Tochigi (Japan)

    1999-04-01

    To investigate the role of intercellular adhesion molecule-1 (ICAM-1) in the pathogenesis of radiation pneumonitis and to determine whether the measurement of soluble ICAM-1 (sICAM-1) levels is useful for predicting the onset of pneumonitis, the levels of sICAM-1 were measured in serum and broncholveolar lavage (BAL) fluids from patients with lung malignancy who received radiotherapy. A total of 30 patients were irradiated with a total dose of {approx}60 Gy. Blood samples were taken before, midway and after radiotherapy. BAL was also performed before and after radiotherapy in seven cases. The sICAM-1 concentration was measured using an enzyme-linked immunosorbent assay kit with two different monoclonal antibodies. Twelve out of 30 cases developed radiation pneumonitis (pneumonitis group), and the other cases did not (non-pneumonitis group). Serum levels of sICAM-1 after radiotherapy were significantly elevated in the pneumonitis group, but not in the non-pneumonitis group. In some of the cases in the pneumonitis group, sICAM-1 levels began to increase at an early phase of irradiation. In one case of pneumonitis in which BAL was performed, the total cell count and the number of lymphocytes increased markedly, as did the level of sICAM-1 in BAL fluid. These findings suggest that intercellular adhesion molecule-1 may play an important role in the development of radiation pneumonitis and that soluble intercellular adhesion molecule-1 may be a useful marker for the early detection of radiation pneumonitis. (au) 29 refs.

  17. Intercellular adhesion molecule 1 promotes HIV-1 attachment but not fusion to target cells.

    Directory of Open Access Journals (Sweden)

    Naoyuki Kondo

    Full Text Available Incorporation of intercellular adhesion molecule 1 (ICAM-1 into HIV-1 particles is known to markedly enhance the virus binding and infection of cells expressing lymphocyte function-associated antigen-1 (LFA-1. At the same time, ICAM-1 has been reported to exert a less pronounced effect on HIV-1 fusion with lymphoid cells. Here we examined the role of ICAM-1/LFA-1 interactions in productive HIV-1 entry into lymphoid cells using a direct virus-cell fusion assay. ICAM-1 promoted HIV-1 attachment to cells in a temperature-dependent manner. It exerted a marginal effect on virus binding in the cold, but enhanced binding up to 4-fold at physiological temperature. ICAM-1-independent attachment in the cold was readily reversible upon subsequent incubation at elevated temperature, whereas ICAM-1-bearing particles were largely retained by cells. The better virus retention resulted in a proportional increase in HIV-1 internalization and fusion, suggesting that ICAM-1 did not specifically accelerate endocytosis or fusion steps. We also measured the rates of CD4 engagement, productive endocytosis and HIV-endosome fusion using specific fusion inhibitors. These rates were virtually independent of the presence of ICAM-1 in viral particles. Importantly, irrespective of the presence of ICAM-1, HIV-1 escaped from the low temperature block, which stopped virus endocytosis and fusion, much later than from a membrane-impermeant fusion inhibitor targeting surface-accessible particles. This result, along with the complete inhibition of HIV-1 fusion by a small molecule dynamin inhibitor, implies this virus enters lymphoid cells used in this study via endocytosis and that this pathway is not altered by the viral ICAM-1. Our data highlight the role of ICAM-1 in stabilizing the HIV-1 attachment to LFA-1 expressing cells, which leads to a proportional enhancement of the receptor-mediated uptake and fusion with endosomes.

  18. 虎杖甙对脂多糖诱导血管内皮细胞ICAM-1表达的抑制作用%Inhibiting role of polydatin to expression of intercellular adhesion molecule- 1 induced by lipopolysaccharide on vascular endothelial cells

    Institute of Scientific and Technical Information of China (English)

    闫文生; 赵克森; 姜勇; 王静珍

    2001-01-01

    目的和方法:用细胞免疫荧光染色和激光共聚焦显微镜扫描技术,研究脂多糖(LPS)对人脐静脉内皮细胞(HUVEC)细胞间粘附分子-1(ICAM-1)表达的诱导作用,以及虎杖甙对ICAM-1表达的抑制作用.结果:内皮细胞未受LPS刺激时,细胞表面ICAM-1表达很弱;LPS刺激后,细胞表面ICAM-1分子在第8-36h显著增加,并与ICAM-1的表达呈剂量反应关系.虎杖甙单独处理内皮细胞时,对ICAM-1表达无明显影响;但虎杖甙预处理内皮细胞后,可显著抑制LPS对ICAM-1表达的诱导作用.结论:LPS可促进内皮细胞ICAM-1的表达,并可被虎杖甙所抑制.

  19. Soluble adhesion molecules ICAM-1, VCAM-1, P-selectin in children with Helicobacter pylori infection

    Institute of Scientific and Technical Information of China (English)

    Elzbieta Maciorkowska; Maciej Kaczmarski; Anatol Panasiuk; Katarzyna Kondej-Muszynska; Andrzej Kemonai

    2005-01-01

    AIM: To assess the sICAM-1, sVCAM-1, and sP-selectin levels in children withHelicobacter pylori(H pylori)infection and to evaluate their significance for the morphological changes found in gastric mucosa.METHODS: The study included 106 children: 59children (55.7%) with chronic gastritis and positive IgG against H pylori, 29 children (27.3%) after previous H pylori infection without the bacterium colonization but with positive IgG against H pylori, and 18 children (17%) with functional disorders of the gastrointestinal system but with normal IgG against H pylori. Endoscopic and histopathological evaluation of gastric mucosa was performed based on the Sydney System classification.The evaluation of sP-selectin, sIC AM-1, sVCAM-1 levels in the sera of children was carried out using ELISA test.RESULTS: The assessment of gastritis activity degrees indicated statistically significant values in the antrum and corpus (P<0.001) of children examined. Serum sVCAM-1 levels were higher in group with gastritis due to H pylori infection than in group without infection and differed statistically (P<0.05). Serum sVCAM-1 levels proved to be the highest among other adhesive molecules in infected children and decreased after eradication of H pylori. Serum sICAM-1 levels were similar in all examined groups. Serum sP-selectin levels were similar in children with and without H pylori infection.CONCLUSION: Assessment of adhesive molecules (sPselectin, sICAM-1, sVCAM-1) in the sera of children with active H pylori infection can show the participation of sVCAM-1 in the pathogenesis of gastric mucosal inflammation, sP-selectin and sICAM-1 concentrations in the sera of children with H pylori infection after eradication cannot reveal any significant differences as compared to healthy children.

  20. Intercellular Cell Adhesion Molecule-1, Vascular Cell Adhesion Molecule-1, and Regulated on Activation Normal T Cell Expressed and Secreted Are Expressed by Human Breast Carcinoma Cells and Support Eosinophil Adhesion and Activation

    OpenAIRE

    Ali, Shahina; Kaur, Jaswinder; Patel, Kamala D.

    2000-01-01

    Eosinophils are usually associated with parasitic and allergic diseases; however, eosinophilia is also observed in several types of human tumors, including breast carcinomas. In this study we examined several human breast carcinoma cell lines for adhesion molecule expression and the ability to bind and activate eosinophils. MDA-MB-435S and MDA-MB-468 cells constitutively expressed both intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) and this expressio...

  1. Detection of soluble intercellular adhesion molecule-1 in serum of children with virus-associated wheezing bronchitis and correlation analysis with breathing-related risk factors%病毒相关性喘息性支气管炎患儿血清sICAM-1的检测及其与喘息高危因素的相关性分析

    Institute of Scientific and Technical Information of China (English)

    莫蔚农; 徐嘉望; 王红旗

    2012-01-01

    目的:探讨血清可溶性细胞间粘附分子-1(sICAM-1)在病毒相关性喘息性支气管炎发病中的作用,分析血清sICAM-1水平与喘息反复发作的高危因素者之间的关系.方法:采用酶联免疫吸附试验方法测定70例病毒相关性喘息性支气管炎急性期和恢复期以及30例健康儿童血清sICAM-1水平,分析病毒相关性喘息性支气管炎喘息反复发作的可能相关因素.结果:急性期血清sICAM-1水平高于恢复期和对照组,差异有统计学意义(P<0.05);恢复期血清sICAM-1水平与对照组比较差异无统计学意义(P>0.05).随访期内有23例患儿喘息反复发作,其血清sICAM-1水平为(218.94 ±60.82) ng/ml.有过敏性疾病史和遗传史患儿血清sICAM-1水平显著高于无过敏性疾病史和遗传史患儿,差异有统计学意义(P<0.05).结论:血清sICAM-1参与了病毒相关性喘息性支气管炎发生和发展以及喘息复发,有过敏性疾病和遗传史病毒感染所致的喘息性支气管炎患儿易喘息反复发作.%Objective: To explore the effect of serum soluble intercellular adhesion molecule — 1 ( sICAM - 1) in the occurrence of virus — associated wheezing bronchitis, and analyze the relationship between sICAM - 1 and high risk factors of repeated onset of wheezing. Methods: Enzyme -linked immunosorbent assay (ELISA) was used to detect the serum levels of sICAM - 1 in 70 children with virus — associated wheezing bronchitis at acute phase and recovery phase and 30 healthy children , the probable related factors of repeated onset of virus — associated wheezing bronchitis were analyzed. Results: The serum level of sICAM — 1 in children with virus — associated wheezing bronchitis at acute was significantly higher than those in case group at recovery phase and control group, there was statistically significant difference (P 0. 05) . During follow — up period, wheezing occurred repeatedly in 23 children, and the serum level of s

  2. Detection of Expressed Intercellular Adhesion Molecule - 1 and HLA - DR and Lymphocyte Function Association Antigen - 1 in Lesions of Exanthematous Drug Eruption by Immunohistochemistry%用免疫组化法对发疹型药疹皮损中ICAM-1和HLA-DR及LFA-1的检测

    Institute of Scientific and Technical Information of China (English)

    段昕所; 陆洁; 胡晓梅; 白亚来; 张春雷; 李世荫

    2000-01-01

    目的探讨细胞间粘附分子-1(ICAM-1)和人类白细胞表面抗原-DR(HLA-DR)及淋巴细胞功能相关抗原-1(LFA-1)在发疹型药疹发病机制中的作用.方法用免疫组化LSAB法对34例发疹型药疹患者皮损组织和8例对照皮肤中ICAM-1和HIA-DR及LFA-1进行了检测.结果发现皮损中角质形成细胞表达ICAM-1和HLA-DR,其阳性率明显高于8例正常对照,在真皮的血管内皮细胞也有ICAM-1的表达,真皮浸润淋巴细胞还表达LFA-1.结论 HLA-DR、ICAM-1和LFA-1参与了发疹型药疹的炎症过程.

  3. Retinal Vascular Endothelial Growth Factor Induces Intercellular Adhesion Molecule-1 and Endothelial Nitric Oxide Synthase Expression and Initiates Early Diabetic Retinal Leukocyte Adhesion in Vivo

    OpenAIRE

    Joussen, Antonia M; Poulaki, Vassiliki; Qin, Wenying; Kirchhof, Bernd; Mitsiades, Nicholas; Wiegand, Stanley J.; Rudge, John; Yancopoulos, George D.; Adamis, Anthony P.

    2002-01-01

    Leukocyte adhesion to the diabetic retinal vasculature results in early blood-retinal barrier breakdown, capillary nonperfusion, and endothelial cell injury and death. Previous work has shown that intercellular adhesion molecule-1 (ICAM-1) and CD18 are required for these processes. However the relevant in vivo stimuli for ICAM-1 and CD18 expression in diabetes remain unknown. The current study investigated the causal role of endogenous vascular endothelial growth factor (VEGF) and nitric oxid...

  4. Study on the Expressions of Plasma Soluble Thrombomodulin and Soluble Intercellular Adhesion Molecule-1 in Acute Coronary Syndrome%血浆sTM和sICAM-1在急性冠脉综合征患者中的表达

    Institute of Scientific and Technical Information of China (English)

    陈欣; 张广枚; 江燕; 蔡林; 王彦欧; 郭素箴; 党群

    2006-01-01

    目的:探讨血浆可溶性血栓调节蛋白(sTM)和可溶性细胞间黏附因子-1(sICAM-1)的水平在急性冠脉综合征患者(ACS组)发病中的作用.方法:用酶联免疫吸附法测定ACS组及对照组血浆sTM及sICAM-1的水平.结果:ACS组sTM水平低于对照组(P<0.01),其中AMI组sTM水平高于UAP组,但差异无统计学意义(P>0.05);sICAM-1水平AMI组高于对照组和UAP组(均P<0.01).AMI组sTM与sICAM-1呈正相关(r=0.656,P<0.01),sTM及sICAM-1与肌钙蛋白I(TnI)呈正相关(r分别为0.453和0.34,均P<0.01).结论:sTM、sICAM-1水平是反映ACS患者内皮细胞损伤程度和范围的良好标志.炎症反应、内皮损伤在ACS发生过程中起协同作用,炎症反应促进了急性血栓形成.

  5. Serum levels of thrombomodulin, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and E-selectin in the acute phase of Plasmodium vivax malaria.

    Science.gov (United States)

    Ohnishi, K

    1999-02-01

    Elevated plasma or serum levels of thrombomodulin (TM), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin have been reported in several diseases. However, plasma or serum levels of TM, ICAM-1, VCAM-1, and E-selectin have not been investigated in the acute phase of Plasmodium vivax malaria. Serum TM, ICAM-1, VCAM-1, E-selectin, and creatinine levels were determined in six Japanese patients in the acute phase of vivax malaria and in seven healthy Japanese controls. Parasitemias of the peripheral blood were Fujirebio units/ml, 709 +/- 397 ng/ml, 2,112 +/- 782 ng/ml, and 99 +/- 28 ng/ml, respectively, and all were significantly greater than those in the controls (TM; P < 0.005, ICAM-1; P < 0.025, VCAM-1; P < 0.005, E-selectin; P < 0.025). However, no significant difference was identified between patients and controls for serum creatinine values. The serum levels of TM and VCAM-1 were not related to parasitemia. The elevation of serum TM levels suggests that endothelial cell damage occurs in the acute phase of vivax malaria.

  6. Lipid Raft is required for PSGL-1 ligation induced HL-60 cell adhesion on ICAM-1.

    Directory of Open Access Journals (Sweden)

    Tingshuang Xu

    Full Text Available P-selectin glycoprotein ligand-1 (PSGL-1 and integrins are adhesion molecules that play critical roles in host defense and innate immunity. PSGL-1 mediates leukocyte rolling and primes leukocytes for integrin-mediated adhesion. However, the mechanism that PSGL-1 as a rolling receptor in regulating integrin activation has not been well characterized. Here, we investigate the function of lipid raft in regulating PSGL-1 induced β2 integrin-mediated HL-60 cells adhesion. PSGL-1 ligation with antibody enhances the β2 integrin activation and β2 integrin-dependent adhesion to ICAM-1. Importantly, with the treatment of methyl-β-cyclodextrin (MβCD, we confirm the role of lipid raft in regulating the activation of β2 integrin. Furthermore, we find that the protein level of PSGL-1 decreased in raft fractions in MβCD treated cells. PSGL-1 ligation induces the recruitment of spleen tyrosine kinase (Syk, a tyrosine kinase and Vav1 (the pivotal downstream effector of Syk signaling pathway involved in cytoskeleton regulation to lipid raft. Inhibition of Syk activity with pharmacologic inhibitor strongly reduces HL-60 cells adhesion, implicating Syk is crucial for PSGL-1 mediated β2 integrin activation. Taken together, we report that ligation of PSGL-1 on HL-60 cells activates β2 integrin, for which lipid raft integrity and Syk activation are responsible. These findings have shed new light on the mechanisms that connect leukocyte initial rolling with subsequent adhesion.

  7. Matrix stiffness exerts biphasic control over monocyte-endothelial adhesion via Rho-mediated ICAM-1 clustering.

    Science.gov (United States)

    Scott, Harry A; Quach, Boi; Yang, Xiao; Ardekani, Soroush; Cabrera, Andrea P; Wilson, Randall; Messaoudi-Powers, Ilhem; Ghosh, Kaustabh

    2016-08-01

    Leukocyte-endothelial adhesion is a critical early step in chronic vascular inflammation associated with diabetes, emphysema, and aging. Importantly, these conditions are also marked by abnormal subendothelial matrix crosslinking (stiffness). Yet, whether and how abnormal matrix stiffness contributes to leukocyte-endothelial adhesion remains poorly understood. Using a co-culture of human monocytic cells and human microvascular endothelial cells (ECs) grown on matrices of tunable stiffness, we demonstrate that matrix stiffness exerts biphasic control over monocyte-EC adhesion, with both matrix softening and stiffening eliciting a two-fold increase in this adhesive interaction. This preferential endothelial adhesivity on softer and stiffer matrices was consistent with a significant increase in α-actinin-4-associated endothelial ICAM-1 clustering, a key determinant of monocyte-EC adhesion. Further, the enhanced ICAM-1 clustering on soft and stiff matrices correlated strongly with an increase in Rho activity and ROCK2 expression. Importantly, inhibition of Rho/ROCK activity blocked the effects of abnormal matrix stiffness on ICAM-1 clustering and monocyte-EC adhesion. Thus, these findings implicate matrix stiffness-dependent ICAM-1 clustering as an important regulator of vascular inflammation and provide the rationale for closely examining mechanotransduction pathways as new molecular targets for anti-inflammatory therapy.

  8. Expression of intercellular adhesion molecule-1 in UVA-irradiated human skin cells in vitro and in vivo

    Energy Technology Data Exchange (ETDEWEB)

    Treina, G.; Scaletta, C.; Frenk, E.; Applegate, L.A. [University Hospital-CHUV, Lausanne (Switzerland). Laboratory of Photobiology; Fourtanier, A.; Seite, S. [L`Oreal-Centre de Recherche Charles Zviak (France). Recherche Avancee Biologie

    1996-08-01

    Ultraviolet A (UVA) radiation represents an important oxidative stress to human skin and certain forms of oxidative stress have been shown to modulate intercellular adhesion molecule-1 (ICAM-1) expression. ICAM-1 has been shown to play an important part in many immune reactions and the perturbations of this molecule by ultraviolet radiation could have implications in many inflammatory responses. An enhancement immunohistochemical method with avidin/biotin was used for analysing the early effects of UVA radiation on human cell cultures and human skin (340-400 nm). Both in vitro and in vivo data show that ICAM-1 staining in epidermal keratinocytes, which was expressed constitutively, decreased in a UVA dose-dependent manner. The decrease was most noted at 3-6 h following UVA radiation with some ICAM-1 staining returning by 48 h post-UVA. ICAM-1 positive staining in the dermis was specific for vascular structures and was increased 24 h after UVA radiation. Cultured dermal fibroblasts exhibited ICAM-1 staining which increased slightly within 6-48 h post-UVA radiation. As epidermal ICAM-1 expression is depleted following UVA radiation and dermal expression increases due to an increase in the vascular structures, ICAM-1 provides a valuable marker following UVA radiation in human skin that can be readily measured in situ. (author).

  9. Skeletal muscle cells express ICAM-1 after muscle overload and ICAM-1 contributes to the ensuing hypertrophic response.

    Directory of Open Access Journals (Sweden)

    Christopher L Dearth

    Full Text Available We previously reported that leukocyte specific β2 integrins contribute to hypertrophy after muscle overload in mice. Because intercellular adhesion molecule-1 (ICAM-1 is an important ligand for β2 integrins, we examined ICAM-1 expression by murine skeletal muscle cells after muscle overload and its contribution to the ensuing hypertrophic response. Myofibers in control muscles of wild type mice and cultures of skeletal muscle cells (primary and C2C12 did not express ICAM-1. Overload of wild type plantaris muscles caused myofibers and satellite cells/myoblasts to express ICAM-1. Increased expression of ICAM-1 after muscle overload occurred via a β2 integrin independent mechanism as indicated by similar gene and protein expression of ICAM-1 between wild type and β2 integrin deficient (CD18-/- mice. ICAM-1 contributed to muscle hypertrophy as demonstrated by greater (p<0.05 overload-induced elevations in muscle protein synthesis, mass, total protein, and myofiber size in wild type compared to ICAM-1-/- mice. Furthermore, expression of ICAM-1 altered (p<0.05 the temporal pattern of Pax7 expression, a marker of satellite cells/myoblasts, and regenerating myofiber formation in overloaded muscles. In conclusion, ICAM-1 expression by myofibers and satellite cells/myoblasts after muscle overload could serve as a mechanism by which ICAM-1 promotes hypertrophy by providing a means for cell-to-cell communication with β2 integrin expressing myeloid cells.

  10. Soluble intercellular adhesion molecule-1 for stable and acute phases of idiopathic pulmonary fibrosis.

    Science.gov (United States)

    Okuda, Ryo; Matsushima, Hidekazu; Aoshiba, Kazutetsu; Oba, Tomohiro; Kawabe, Rie; Honda, Koujiro; Amano, Masako

    2015-01-01

    The levels of soluble intercellular adhesion molecule-1 (sICAM-1) have been reported to increase in patients with idiopathic pulmonary fibrosis. However, the utility of sICAM-1 has not been reported in detail. The aim of this study was to investigate whether sICAM-1 was a useful biomarker for stable idiopathic pulmonary fibrosis (IPF) and early phase of acute exacerbation of IPF. The patients who were diagnosed with IPF between 2013 and 2015 were enrolled. The levels of sICAM-1 and other interstitial pneumonia markers were measured. In this study, 30 patients with stable IPF and 11 patients with acute exacerbation of IPF were collected. Mean sICAM-1 levels were 434 ± 139 ng/mL for the stable phase of IPF, 645 ± 247 ng/mL for early phase of acute exacerbation of IPF, 534 ± 223 ng/mL for connective tissue disease-associated interstitial pneumonia, 221 ± 42 for chronic obstructive pulmonary disease, and 150 ± 32 ng/mL in healthy volunteers. For the stable phase of IPF, sICAM-1 levels correlated with Krebs von den Lungen-6 (KL-6) (r value: 0.41; p value: 0.036). Mean sICAM-1 levels were significantly higher in patients with early phase of acute exacerbation of IPF than with stable phase of IPF (p = 0.0199). Multiple logistic analyses indicated that the predictors for early phase of acute exacerbation of IPF were only sICAM-1 and C-reactive protein (odds ratio: 1.0093; 1.6069). In patients with stable IPF, sICAM-1 levels correlated with KL-6; sICAM-1 might be a predictive indicator for prognosis. In the early phase of acute exacerbation of IPF, sICAM-1 might be more useful for diagnosis than other interstitial pneumonia markers. PMID:26543791

  11. ICAM-1-independent, CD18-dependent adhesion between neutrophils and human epithelial cells exposed in vitro to ozone

    Energy Technology Data Exchange (ETDEWEB)

    Tosi, M.F.; Hamedani, A.; Brosovich, J.; Alpert, S.E. (Case Western Reserve Univ. School of Medicine, Cleveland, OH (United States))

    1994-02-15

    Inhalant exposure to ozone can cause diffuse airway epithelial injury that is associated with an inflammatory response, including the influx of neutrophils into lung and airway tissue. The authors have previously documented enhanced adhesiveness by neutrophils for human airway epithelial cells in in vitro models of diseases associated with airway inflammation and have suggested that this enhanced adhesion may contribute to neutrophil-mediated airway injury. When primary human tracheal epithelial cell (TEC) monolayers were exposed to ozone at 2.0 ppm for 30 min or 0.5 ppm for 2 h, the percentage of PMN adhering to these cells increased from <5% to a maximum of approximately 75% by 18 to 24 h after the ozone exposure. No change was observed within the first 2 h after ozone exposure, but there was a statistically significant increase in PMN adhesion by 8 h after exposure. In contrast to previous studies with cytokine exposure or respiratory virus infection of TEC, the increased adhesion after ozone exposure was not associated with an increase in epithelial expression of ICAM-1. Consistent with the lack of induction of ICAM-1 by ozone exposure was the observation that anti-ICAM-1 mAbs previously shown to block PMN adhesion to TEC with increased ICAM-1 expression had no effect on PMN adhesion to ozone-exposed TEC. However, mAbs against CD11b or CD18 on PMN blocked PMN adhesion to ozone-exposed TEC by approximately 55 and 80%, respectively. Chemoattractant preactivation of PMN was necessary to achieve the highest levels of adhesion to ozone-treated TEC, in marked contrast to earlier studies with PMN adhesion to cytokine-treated or virus-infected TEC in which resting and prestimulated PMN exhibited the same high levels of adhesion.

  12. The effect of adhesion molecule ICAM-1 on transplantation immunity%粘附分子ICAM-1在移植免疫中的作用

    Institute of Scientific and Technical Information of China (English)

    娄诚

    2003-01-01

    粘附分子细胞间粘附因子-1(ICAM-1)在器官移植免疫反应中发挥重要作用,是诊断排斥反应灵敏的指标,体液细胞间粘附因子(sICAM-1)的监测对排斥反应的鉴别诊断有重要参考价值,同时应用ICAM-1单克隆抗体进行排斥反应治疗的研究也已取得一定的成果.

  13. Expression of intercellular adhesion molecule-1and HLA-DR antigens in uveitis

    Institute of Scientific and Technical Information of China (English)

    1999-01-01

    目的:研究细胞间粘附分子-1(intellular adhesion molecule-1,ICAM-1)和人体组织相关抗原(human leudocyte antigen,HLA-DR)在萄萄膜炎免疫反应中的作用.方法:应用免疫组织化学染色检查20只正常眼和54例葡萄糖膜炎眼球摘除眼(其中外源性33例和内源性21例)的脉络膜和视网膜组织中ICAM-1和HLA-DR的表达.结果:正常眼的脉络膜和视网膜组织没有ICAM-1的阳性染色,没有或较少有HLA-DR的表达,葡萄膜炎眼中二者有增高表达(P<0.01),而外源性和内源性葡萄膜炎眼组间表达统计学上无显著差异(P>0.05).结论:ICAM-1、HLA-DR分子能够介导白细胞和炎症部位组织细胞的识别和粘附,二者的共同表达说明它们在葡萄糖膜炎脉络膜视网膜组织的免疫性损伤中具有重要意义.%Objective :To study the effects of intercellular adhesion molecule-1 (ICAM-1) and human leukocyte antigen (HAL-DR) on the immunopathologic process of uveitis. Methods:Imn- munohistochemical techniques were applied to detect their expression in eyes of both the health (20 cases from eye bank) and patients with uveitis (54 cases with 54 eyes which included 33 ex- ogenous uveitis and 21 endogenous one). Results:Both the two ant igens were detectable in the choroidal and retinal tissues in eyes of uveitis while all the normal eyes showed negative expres- sion of ICAM-1 and negative or little expression of HLA-DR (P<0. 01). However,there was no statistically significant difference between exogenous and endogenous types (P>0. 05). Conclu- sion: Both ICAM-1 and HLA-DR may be responsible for cell recognition and binding in the in- flarnmatory tissues. The co-expression of ICAM-1 and HAL-DR showed that these two factors might play an important role in the immunologic damage of the choroid and retina in uveitis.

  14. Activation of cord T lymphocytes. III. Role of LFA-1/ICAM-1 and CD2/LFA-3 adhesion molecules in CD3-induced proliferative response.

    Science.gov (United States)

    Gerli, R; Agea, E; Muscat, C; Tognellini, R; Fiorucci, G; Spinozzi, F; Cernetti, C; Bertotto, A

    1993-04-15

    As cord T cells, a model of antigen (Ag)-unprimed cell, display a functional defect when stimulated through the CD3 molecule, the role of lymphocyte function-associated antigen 1(LFA-1)/intercellular adhesion molecule 1 (ICAM-1) and CD2/lymphocyte function-associated antigen 3 (LFA-3) receptor-ligand pairs in cord CD3-triggered T-cell activation was analyzed using specific monoclonal antibodies (mAb) against each adhesion molecule. The addition of anti-CD11a, anti-CD18, or anti-CD2 to both adult and cord peripheral blood mononuclear cells (PBMC) cultures led to a decrease in CD3-induced proliferation. In contrast, CD3-stimulated cord, but not adult, PBMC proliferation was markedly enhanced when anti-CD54 or anti-CD58 were added. Despite the fact that ICAM-1 and LFA-3 molecules were virtually absent on cord resting T cells, mAb against these two molecules boosted both mitogenesis of and interleukin (IL)-2 production by purified cord T cells stimulated with plastic immobilized anti-CD3. Cord T-cell supernatant levels of interferon-gamma (IFN-gamma) were undetectable with CD3 stimulation, slightly raised with CD58/CD3 costimulation, but normal when T cells were preincubated with IL-2 for 24 hr before being costimulated with anti-CD3/CD58. Evidence that IL-2 and IFN-gamma play a pivotal role in fully activating cord T cells came from the demonstration that IL-2 and IFN-gamma are able to bypass the CD3-proliferative defect through differential up-regulation of the adhesion molecules. It would, therefore, seem that ICAM-1 and LFA-3 molecules are crucially implicated in the CD3-activation pathway of Ag-unprimed T cells. PMID:7684326

  15. Soluble fms-like tyrosine kinase-1 and endothelial adhesion molecules (intercellular cell adhesion molecule-1 and vascular cell adhesion molecule-1) as predictive markers for blood pressure reduction after renal sympathetic denervation.

    Science.gov (United States)

    Dörr, Oliver; Liebetrau, Christoph; Möllmann, Helge; Gaede, Luise; Troidl, Christian; Rixe, Johannes; Hamm, Christian; Nef, Holger

    2014-05-01

    Renal sympathetic denervation (RSD) is a treatment option for patients with resistant arterial hypertension, but in some patients it is not successful. Predictive parameters on the success of RSD remain unknown. The angiogenic factors soluble fms-like tyrosine kinase-1 (sFLT-1), intercellular cell adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) are known to be associated with endothelial dysfunction, vascular remodeling, and hypertension. We evaluated whether sFLT-1, ICAM-1, and VCAM-1 are predictive markers for blood pressure reduction after RSD. Consecutive patients (n=55) undergoing renal denervation were included. Venous serum samples for measurement of sFlt-1, ICAM-1, and VCAM-1 were collected before and 6 months after RSD. A therapeutic response was defined as an office systolic blood pressure reduction of >10 mm Hg 6 months after RSD. A significant mean office systolic blood pressure reduction of 31.2 mm Hg was observed in 46 patients 6 months after RSD. Nine patients were classified as nonresponders, with a mean systolic blood pressure reduction of 4.6 mm Hg. At baseline, sFLT-1 levels were significantly higher in responders than in nonresponders (P<0.001) as were ICAM-1 (P<0.001) and VCAM-1 levels (P<0.01). The areas under the curve for sFLT-1, ICAM-1, and VCAM-1 were 0.82 (interquartile range, 0.718-0.921; P<0.001), 0.754 (0.654-0.854; P<0.001), and 0.684 (0.564-804; P=0.01), respectively, demonstrating prediction of an RSD response. Responders showed significantly higher serum levels of sFLT-1, ICAM-1, and VCAM-1 at baseline compared with nonresponders. Thus, this study identified for the first time potential biomarkers with a predictive value indicating a responder or nonresponder before renal denervation. PMID:24470464

  16. Intercellular adhesion molecule 1 serves as a primary cognate receptor for the Type IV pilus of nontypeable Haemophilus influenzae.

    Science.gov (United States)

    Novotny, Laura A; Bakaletz, Lauren O

    2016-08-01

    Nontypeable Haemophilus influenzae (NTHI) utilizes the Type IV pilus (Tfp) to adhere to respiratory tract epithelial cells thus colonizing its human host; however, the host cell receptor to which this adhesive protein binds is unknown. From a panel of receptors engaged by Tfp expressed by other bacterial species, we showed that the majority subunit of NTHI Tfp, PilA, bound to intercellular adhesion molecule 1 (ICAM1) and that this interaction was both specific and of high affinity. Further, Tfp-expressing NTHI inoculated on to polarized respiratory tract epithelial cells that expressed ICAM1 were significantly more adherent compared to Tfp-deficient NTHI or NTHI inoculated on to epithelial cells to which ICAM1 gene expression was silenced. Moreover, pre-incubation of epithelial cells with recombinant soluble PilA (rsPilA) blocked adherence of NTHI, an outcome that was abrogated by admixing rsPilA with ICAM1 prior to application on to the target cells. Epithelial cells infected with adenovirus or respiratory syncytial virus showed increased expression of ICAM1; this outcome supported augmented adherence of Tfp-expressing NTHI. Collectively, these data revealed the cognate receptor for NTHI Tfp as ICAM1 and promote continued development of a Tfp-targeted vaccine for NTHI-induced diseases of the airway wherein upper respiratory tract viruses play a key predisposing role.

  17. Expression of ICAM-1 in colon epithelial cells

    DEFF Research Database (Denmark)

    Vainer, Ben; Sørensen, Susanne; Seidelin, Jakob;

    2003-01-01

    Studies have suggested that in ulcerative colitis (UC), intercellular adhesion molecule-1 (ICAM-1) is involved in migration of leukocytes toward the colonic epithelium. A suitable in vitro model of chronic colonic inflammation does not exist, and the role of the epithelium is based on monolayers...... of cancer cells. Conflicting results exist on epithelial ICAM-1 expression, and the aim of this study was to compare the expression in various models of colonic epithelium....

  18. Fructose Induces the Inflammatory Molecule ICAM-1 in Endothelial Cells

    OpenAIRE

    Glushakova, Olena; Kosugi, Tomoki; Roncal, Carlos; Mu, Wei; Heinig, Marcelo; Cirillo, Pietro; Sánchez-Lozada, Laura G.; Richard J Johnson; Nakagawa, Takahiko

    2008-01-01

    Epidemiologic studies have linked fructose intake with the metabolic syndrome, and it was recently reported that fructose induces an inflammatory response in the rat kidney. Here, we examined whether fructose directly stimulates endothelial inflammatory processes by upregulating the inflammatory molecule intercellular adhesion molecule-1 (ICAM-1). When human aortic endothelial cells were stimulated with physiologic concentrations of fructose, ICAM-1 mRNA and protein expression increased in a ...

  19. Hyperketonemia (Acetoacetate Upregulates NADPH Oxidase 4 and Elevates Oxidative Stress, ICAM-1, and Monocyte Adhesivity in Endothelial Cells

    Directory of Open Access Journals (Sweden)

    Preeti Kanikarla-Marie

    2015-01-01

    Full Text Available Background/Aims: The incidence of developing microvascular dysfunction is significantly higher in type 1 diabetic (T1D patients. Hyperketonemia (acetoacetate, β-hydroxybutyrate is frequently found along with hyperglycemia in T1D. Whether hyperketonemia per se contributes to the excess oxidative stress and cellular injury observed in T1D is not known. Methods: HUVEC were treated with ketones in the presence or absence of high glucose for 24 h. NOX4 siRNA was used to specifically knockdown NOX4 expression in HUVEC. Results: Ketones alone or in combination with high glucose treatment cause a significant increase in oxidative stress, ICAM-1, and monocyte adhesivity to HUVEC. Using an antisense approach, we show that ketone induced increases in ROS, ICAM-1 expression, and monocyte adhesion in endothelial cells were prevented in NOX4 knockdown cells. Conclusion: This study reports that elevated levels of ketones upregulate NOX, contributing to increased oxidative stress, ICAM-1 levels, and cellular dysfunction. This provides a novel biochemical mechanism that elucidates the role of hyperketonemia in the excess cellular injury in T1D. New drugs targeting inhibition of NOX seems promising in preventing higher risk of complications associated with T1D.

  20. Actin-binding proteins differentially regulate endothelial cell stiffness, ICAM-1 function and neutrophil transmigration

    NARCIS (Netherlands)

    Schaefer, A.; Riet, J. te; Ritz, K.; Hoogenboezem, M.; Anthony, E.C.; Mul, F.P.; Vries, C.J. de; Daemen, M.J.; Figdor, C.G.; Buul, J.D. van; Hordijk, P.L.

    2014-01-01

    Chronic vascular inflammation is driven by interactions between activated leukocytes and the endothelium. Leukocyte beta2-integrins bind to endothelial intercellular adhesion molecule 1 (ICAM-1), which allows leukocyte spreading, crawling and transendothelial migration. Leukocytes scan the vascular

  1. Association of ICAM-1 K469E polymorphism with neurocysticercosis.

    Science.gov (United States)

    Singh, Amrita; Singh, Aloukick K; Singh, Satyendra K; Paliwal, Vimal K; Gupta, Rakesh K; Prasad, Kashi N

    2014-11-15

    Neurocysticercosis (NCC), a central nervous system (CNS) disease is caused by the larval stage of Taenia solium. The disease is heterogeneous in clinical presentation; some infected individuals develop symptoms and others may remain symptom free. Impaired blood brain barrier allows recruitment of immune cells in the CNS during infection and soluble intercellular adhesion molecule-1 (sICAM-1) plays an important role in the recruitment of immune cells. We studied ICAM-1 K469E polymorphism among symptomatic and asymptomatic NCC patients. The study revealed that individuals with variant (EE) genotype were more susceptible to symptomatic NCC and also had an elevated level of sICAM-1.

  2. Cardiotrophin-1 induces intercellular adhesion molecule-1 expression by nuclear factor κB activation in human umbilical vein endothelial cells

    Institute of Scientific and Technical Information of China (English)

    2008-01-01

    Background In addition to elevated concentrations of cytokines, patients with congestive heart failure (CHF) show endothelial dysfunction and increased plasma concentrations of adhesion molecules like intercellular adhesion molecule-1 (ICAM-1). Furthermore, the concentration of cardiotrophin-1 (CT-1) - a cytokine of the interleukin-6 superfamily - is increased in CHF. We tested the hypothesis whether CT-1 is able to induce ICAM-1 in human umbilical vein endothelial cells (HUVEC). Furthermore we examined the signalling mechanisms of CT-1 mediated ICAM-1 expression. Methods Confluent layers of HUVEC were incubated with increasing concentrations of CT-1 (5 to 100 ng/ml) for different periods. ICAM-1 mRNA was determined by real-time polymerase chain reaction (PCR) and ICAM-1 surface expression by fluorescence-activated cell sorter (FACS) analysis and soluble ICAM-1 (slCAM-1) in the culture supematant by enzyme linked immunosorbent assay (ELISA). To clarify the signalling pathway of CT-1 induced ICAM-1 expression we used various inhibitors of possible signal transducing molecules, electromobility shift assay (EMSA) and Western blot analysis. Results CT-1 induced ICAM-1 mRNA (1.8i-0.8 fold increase compared to unstimulated cells after 6 hours) and protein (1.4~-0.2 fold increase compared to unstimulated cells after 48 hours) in HUVEC in a time- and concentration-dependent manner. EMSA experiments show that CT-1 causes nuclear factor (NF) KB activation. Because parthenolide could inhibit CT-1 induced ICAM-1 expression NFKB activation is required in this pathway. CT-1 did not activate extraceUular signal regulated kinases (ERK), c-Jun N-terminal kinase (JNK) and p38. Conclusion CT-1 is able to induce ICAM-1 in endothelial cells by NFKB activation. These results may explain in part elevated ICAM-1 concentrations in patients with CHF and endothelial dysfunction.

  3. Clinical evaluation of serum concentrations of intercellular adhesion molecule-1 in patients with colorectal cancer

    Institute of Scientific and Technical Information of China (English)

    Xu Kang; Fang Wang; Jin-Dong Xie; Jun Cao; Pei-Zhong Xian

    2005-01-01

    AIM: To investigate the correlation between the serum soluble intercellular adhesion molecule-1 (sICAM-1) and the clinicopathologic features and to evaluate the possible prognostic significance of sICAM-1 concentration in colorectal cancer.METHODS: A total of 56 patients (mean age 57.3 years)having transitional cell carcinoma of the colorectal and 25 control patients (mean age 42.6 years) were enrolled in the study. The serum samples of the patients were obtained on the day before surgery. Sera were obtained by centrifugation, and stored at -80 ℃ until assay. Serumconcentrations of ICAM-1 were measured with enzymelinked immunoassay. Differences between the two groups were analyzed by Student's t-test.RESULTS: No significant increase of serum sICAM-1 could be demonstrated in the Dukes A1 patients (352.63±61.82μg/L) compared to the control group (345.72±49.81 μg/L,P>0.05), Dukes A1 patients (352.63±61.82 μg/L)compared to Dukes A2,3 patients (491.17±86.36 μg/L,P<0.05). Furthermore, the patients with Dukes B had significantly higher serum concentrations of sICAM-1than those of the control group (496.82±93.04 μg/L vs 345.72±49.81 μg/L, P<0.01). Compared with Dukes A2,3,B colorectal cancer patients, patients with more advanced clinical stage (Dukes C and D) had higher levels of sICAM-1 (743.68±113.74 μg/L vs491.17±86.36 μg/L and 496.82±93.04 μg/L, P<0.001). The difference was statistically significant in sICAM-1 levels between patients with positive lymph node status and those without lymph node involvement (756.25±125.57 μg/L vs445.62±69.18 μg/L, P<0.001).Patients with poorly differentiated colorectal cancer had a higher level of sICAM-1 than those with differentiated and highly differentiated cancer (736.49±121.97 μg/Lvs 410.23±67.47 μg/L, P<0.001).CONCLUSION: In this study, serum ICAM-1 levels were found to be related to tumor presence, clinical stages,and grade. Increased ICAM-1 in patients with colorectal cancer which should

  4. Interaction between Endothelial Protein C Receptor and Intercellular Adhesion Molecule 1 to Mediate Binding of Plasmodium falciparum-Infected Erythrocytes to Endothelial Cells

    Science.gov (United States)

    Avril, Marion; Bernabeu, Maria; Benjamin, Maxwell; Brazier, Andrew Jay

    2016-01-01

    ABSTRACT Intercellular adhesion molecule 1 (ICAM-1) and the endothelial protein C receptor (EPCR) are candidate receptors for the deadly complication cerebral malaria. However, it remains unclear if Plasmodium falciparum parasites with dual binding specificity are involved in cytoadhesion or different parasite subpopulations bind in brain microvessels. Here, we investigated this issue by studying different subtypes of ICAM-1-binding parasite lines. We show that two parasite lines expressing domain cassette 13 (DC13) of the P. falciparum erythrocyte membrane protein 1 (PfEMP1) family have dual binding specificity for EPCR and ICAM-1 and further mapped ICAM-1 binding to the first DBLβ domain following the PfEMP1 head structure in both proteins. As PfEMP1 head structures have diverged between group A (EPCR binders) and groups B and C (CD36 binders), we also investigated how ICAM-1-binding parasites with different coreceptor binding traits influence P. falciparum-infected erythrocyte binding to endothelial cells. Whereas levels of binding to tumor necrosis factor alpha (TNF-α)-stimulated endothelial cells from the lung and brain by all ICAM-1-binding parasite lines increased, group A (EPCR and ICAM-1) was less dependent than group B (CD36 and ICAM-1) on ICAM-1 upregulation. Furthermore, both group A DC13 parasite lines had higher binding levels to brain endothelial cells (a microvascular niche with limited CD36 expression). This study shows that ICAM-1 is a coreceptor for a subset of EPCR-binding parasites and provides the first evidence of how EPCR and ICAM-1 interact to mediate parasite binding to both resting and TNF-α-activated primary brain and lung endothelial cells. PMID:27406562

  5. Expression of ICAM-1 in colon epithelial cells

    DEFF Research Database (Denmark)

    Vainer, Ben; Sørensen, Susanne; Seidelin, Jakob;

    2003-01-01

    Studies have suggested that in ulcerative colitis (UC), intercellular adhesion molecule-1 (ICAM-1) is involved in migration of leukocytes toward the colonic epithelium. A suitable in vitro model of chronic colonic inflammation does not exist, and the role of the epithelium is based on monolayers ...... of cancer cells. Conflicting results exist on epithelial ICAM-1 expression, and the aim of this study was to compare the expression in various models of colonic epithelium.......Studies have suggested that in ulcerative colitis (UC), intercellular adhesion molecule-1 (ICAM-1) is involved in migration of leukocytes toward the colonic epithelium. A suitable in vitro model of chronic colonic inflammation does not exist, and the role of the epithelium is based on monolayers...

  6. A human/mouse chimeric monoclonal antibody against intercellular adhesion molecule-1 for tumor radioimmunoimaging

    Energy Technology Data Exchange (ETDEWEB)

    Yamamura, Miyuki; Hinoda, Yuji; Sasaki, Shigeru; Tsujisaki, Masayuki; Imai, Kohzoh [Sapporo Medical Univ. (Japan); Oriuchi, Noboru; Endo, Keigo

    1996-04-01

    A mouse-human chimeric antibody for intercellular adhesion molecule-1 (ICAM-1) was established by using heavy chain loss mouse mutant hybridoma and human immunoglobulin expression vector. The HA58 hybridoma secreted anti-ICAM-1 monoclonal antibody (MoAb) (IgG1,{kappa}). The gene of the mouse variable region of heavy chain was amplified and cloned by the polymerase chain reaction technique directly from the HA58 hybridoma RNA. The variable region of heavy chain was joined with an expression vector which contains human {gamma}1 constant gene. The expression vector was transfected into heavy chain loss mutant cells HA58-7, which produced only murine immunoglobulin light chains. The resultant chimeric MoAb HA58, chHA58, retained full-binding reactivity to ICAM-1 compared with murine HA58 parental antibody. The chimeric MoAb chHA58 showed little antibody dependent cell-mediated cytotoxic activity against cultured tumor cells. Biodistribution studies with {sup 99m}Tc-labeled chHA58 in nude mice bearing human gastric carcinoma JRST cells, demonstrated that the tumor-blood ratio was 1.55 at 18 h after injection, when the tumors were clearly visible in gamma scintigraphy. These data suggest that chHA58 may be of practical use for radioimmunoimaging of a wide variety of tumors. (author).

  7. Correlation of Serum Concentrations of Soluble Thrombomodulin, Soluble Vascular Cell Adhesion Molecule-1,Intracellular Adhesion Molecule -1 And E-Selectin In Patients WithSystemic Lupus Erythematosus

    Directory of Open Access Journals (Sweden)

    Malak., A. Mohsen*, Magda.A.Gamil*,Maha. I.Shehata

    2003-09-01

    Full Text Available To date no specific serological parameters are available to assess disease activity in systemic lupus erythematosus (SLE. The objective of this study was to correlate serum levels of thrombomodulin (TM, intracellular adhesion molecule-1 sICAM-1, vascular cell adhesion molecule-1 sVCAM-1, and E-selectin with standard laboratory tests and clinical indices of disease activity in 40 patients with SLE and 20 apparently healthy persons as controls. According to British Isles Lupus Assessment Group (BILAG disease activity index, the 40 patients were divided into two groups, the first consisted of 22 with active disease, and the second consisted of 18 patients with inactive SLE. Serum sTM, sICAM-1, sVCAM-I, and E-selectin were measured in their sera, using enzyme linked immuonosorbent assay (ELISA technique.C-reactiv protein (CRP, Erythrocyte sedimentation rates (ESR and serum creatinines were measured by standard laboratory tests. Total leukocytic count and hemoglobin concentration were detected by coulter counter. Levels of sTM and sVCAM were highly elevated in the group of patients with active SLE as compared to the inactive one (P0.05. In SLE, the BILAG disease activity index, ESR and serum creatinine correlated best with sTM, sVCAM-1 and E-selectin levels while there was a weak association between CRP levels and the adhesion molecules, and no correlation between CRP level and disease activity. In conclusion, sTM and sVCAM were the most important serological indices of disease activity in SLE and might be valuable serological parameters for monitoring therapy.

  8. Effects of alpha-tocopherol on superoxide production and plasma intercellular adhesion molecule-1 and antibodies to oxidized LDL in chronic smokers

    NARCIS (Netherlands)

    Tits, van L.J.; Waart, de F.; Hak-Lemmers, H.L.M.; Heijst, P.; Graaf, de J.; Demacker, P.N.; Stalenhoef, A.F.

    2001-01-01

    Antioxidants have been postulated to exert beneficial effects in atherosclerosis. Atherosclerosis is associated with raised plasma levels of soluble intercellular adhesion molecule-1 (sICAM-1) and autoantibodies against oxidized low-density lipoprotein (oxLDL). It is not known whether antioxidants a

  9. Interferon-gamma and interleukin-4 differentially regulate ICAM-1 and VCAM-1 expression on human lung fibroblasts

    NARCIS (Netherlands)

    Spoelstra, FM; Postma, DS; Hovenga, H; Noordhoek, JA; Kauffman, HF

    1999-01-01

    The expression of the adhesion molecules intercellular adhesion molecule-1 (ICAM-1) and more specifically vascular adhesion molecule-1 (VCAM-1) on lung fibroblasts may be important for migration of inflammatory cells through the submucosa to the airway lumen in the asthmatic inflammatory response. T

  10. Serum Soluble Intercellular Adhesion Molecule-1 Level in Acute Lymphoblastic Leukemia in Children

    International Nuclear Information System (INIS)

    Impaired migration of leucocytes is a characteristic feature of leukemia. Knowledge of the mechanisms of leukemic cells migration has expanded greatly in recent years. Leukocyte infiltrates are formed in surrounding tissues due to changes in chemokines and adhesion molecules concentrations. The present study included 45 patients with acute lymphoblastic leukemia (ALL). The mean of their ages was 6.10±4.39 years. They were 29 males and 16 females. They were chosen from those attending the Oncology Clinic and inpatient wards of the National Cancer Institute, Cairo University. They were classified into 3 groups according to the disease activity: Group I: Comprised 15 newly diagnosed cases of ALL. Group II: Consisted of 15 cases of ALL during relapse period. Group III included 15 cases of ALL during complete remission. Also, 15 apparently healthy children with matched age and sex as a control group (group IV). All the studied cases were subjected to thorough clinical examination as well as the following investigations: complete blood picture, bone marrow biopsy and estimation of serum intercellular adhesion molecule-1 (sICAM-1) by ELISA.The results of this study revealed that serum ICAM-l showed no significant changes in its value on comparing group I (newly diagnosed cases) and group II (cases during relapse). On the other hand, a significant higher level of sICAM-1 was observed on comparing groups I and II with group III (cases during remission) separately (P0.05).From this it was concluded that the levels of serum soluble intercellular circulating adhesion molecule ICAM-1 can be utilized for monitoring disease activity of ALL and its response to treatment, as well as for early detection of relapse.

  11. A study of soluble intercellular adhesion molecule-1 in sera of patients with thyroid diseases

    International Nuclear Information System (INIS)

    Objective: Markedly elevated serum soluble intercellular adhesion molecule 1 (sICAM-1) level has recently been reported in patients with autoimmune thyroid disease (AITD). The aim of this study was to investigate the clinical significance of sICAM-1 serum level in patients with different thyroid diseases. Methods: A total of 616 patients were recruited, consisting of 557 Graves' disease (CD), 33 untreated Hashimoto's thyroiditis (HT), 17 untreated simple goiter (SG) and 9 nontoxic nodular goiter (NTNG). Control was a group of 273 healthy individuals with no prior history of thyroid disease. Their serum sICAM-1 levels were measured by 125I-sICAM-1 radioimmunoassay. If sICAM-1 levels of every group fit normal distribution, statistical difference was calculated by ANOVA or t-test; if not, then rank sum test (Kruskal-Wallis or Mann-Whitney) was used. Results: There was no statistically significant difference among the SG [(173.82 ± 59.50) μg/L], NTNG [(159.31 ± 28.73) μg/L] and control [(149.89 ± 39.45) μg/L] groups; whereas the levels in both untreated GD [(255.04 ± 82.40) μg/L] and HT[(227.22 ± 77.08) μg/L] groups were elevated and statistically significant by comparison with the control group (Z=-9.401, -5.902, respectively; both with P 2=88.257, P<0.01). In stable euthyroid patients receiving ATD, a steady trend of gradual decline in sICAM-1 levels was found. When ATD treatment lasted ≥19 months, the sICAM-1 levels in GD patients with and without ophthalmopathy [(211.58 ± 53.58) μg/L and (189.50 ± 39.99) μg/L, respectively] were significantly decreased when compared with the corresponding pair of new-onset groups [(287.36 ± 79.20) μg/L and (244.75 ± 81.58) μg/L, F=9.986, 3.398, respectively; all P<0.05] but remained persistently elevated over the control group even after stopping ATD treatment (Z=-3.813, P<0.05). Conclusions: The sICAM-1 assay is of great importance in the diagnosis of AITD and detection of the associated abnormal immune status

  12. Nitric oxide pretreatment enhances atheroma component highlighting in vivo with intercellular adhesion molecule-1-targeted echogenic liposomes.

    Science.gov (United States)

    Kee, Patrick H; Kim, Hyunggun; Huang, Shaoling; Laing, Susan T; Moody, Melanie R; Vela, Deborah; Klegerman, Melvin E; McPherson, David D

    2014-06-01

    We present an ultrasound technique for the detection of inflammatory changes in developing atheromas. We used contrast-enhanced ultrasound imaging with (i) microbubbles targeted to intercellular adhesion molecule-1 (ICAM-1), a molecule of adhesion involved in inflammatory processes in lesions of atheromas in New Zealand White rabbits, and (ii) pretreatment with nitric oxide-loaded microbubbles and ultrasound activation at the site of the endothelium to enhance the permeability of the arterial wall and the penetration of ICAM-1-targeted microbubbles. This procedure increases acoustic enhancement 1.2-fold. Pretreatment with nitric oxide-loaded echogenic liposomes and ultrasound activation can potentially facilitate the subsequent penetration of targeted echogenic liposomes into the arterial wall, thus allowing improved detection of inflammatory changes in developing atheromas.

  13. Effects of anisodamine on the expressions of vascular endothelial growth factor and intercellular adhesion molecule 1 in experimental infusion phlebitis

    Institute of Scientific and Technical Information of China (English)

    ZHANG Zhen-xiang; WANG Peng; ZHANG Qiu-shi; PAN Xue; ZHAO Qing-xia; WANG Xiao-kai

    2012-01-01

    Background Infusion phlebitis is the most common side effect of clinical intravenous drug therapy and several clinical studies have demonstrated that anisodamine can effectively prevent the occurrence of infusion phlebitis.This study was designed to investigate effects of anisodamine on the expressions of vascular endothelial growth factor (VEGF) and intercellular adhesion molecule 1 (ICAM-1) in a rabbit model of infusion phlebitis and to analyze the mechanisms of anisodamine effect on the prevention and treatment of experimental infusion phlebitis.Methods Twenty-four specific pathogen-free male Japanese white rabbits were randomly assigned to the control group,the model group,the magnesium sulfate group and the anisodamine group.The rabbit model of infusion phlebitis,induced by intravenous administration,was established and expressions of VEGF and ICAM-1 were determined and contrasted with the control group treated with normal saline.We evaluated expression by histopathology,immunohistochemistry,reverse transcription-polymerase chain reaction,and Western blotting assay.Results Pathohistological changes of the model group were observed,such as loss of venous endothelial cells,inflammatory cell infiltration,edema and thrombus.The magnesium sulfate group and the anisodamine group showed significant protective effects on vascular congestion,inflammatory cell infiltration,proliferation,swelling of endothelium and perivascular hemorrhage.The model group showed the highest expressions of VEGF and ICAM-1 of the four groups (P<0.01).On the contrary,anisodamine alleviated the inflammatory damage by significantly reducing the expressions of VEGF and ICAM-1 compared with the model group (P <0.01).There was no significant difference in the expressions of VEGF and ICAM-1 between the magnesium sulfate group and the anisodamine group (P >0.05).Conclusion Anisodamine alleviates inflammatory damage by significantly reducing the expressions of VEGF and ICAM-1,and shows

  14. Combined measurement of soluble and cellular ICAM-1 among children with Plasmodium falciparum malaria in Uganda

    Directory of Open Access Journals (Sweden)

    Cserti-Gazdewich Christine M

    2010-08-01

    Full Text Available Abstract Background Intercellular adhesion molecule-1 (ICAM-1 is a cytoadhesion molecule implicated in the pathogenesis of Plasmodium falciparum malaria. Elevated levels of soluble ICAM-1 (sICAM-1 have previously been reported with increased malaria disease severity. However, studies have not yet examined both sICAM-1 concentrations and monocyte ICAM-1 expression in the same cohort of patients. To better understand the relationship of soluble and cellular ICAM-1 measurements in malaria, both monocyte ICAM-1 expression and sICAM-1 concentration were measured in children with P. falciparum infection exhibiting a spectrum of clinical severity. Methods Samples were analysed from 160 children, aged 0.5 to 10.8 years, with documented P. falciparum malaria in Kampala, Uganda. The patients belonged to one of three pre-study defined groups: uncomplicated malaria (UM, severe non-fatal malaria (SM-s, and fatal malaria (SM-f. Subset analysis was done on those with cerebral malaria (CM or severe malaria anaemia (SMA. Monocyte ICAM-1 was measured by flow cytometry. sICAM-1 was measured by enzyme immunoassay. Results Both sICAM-1 and monocyte cell-surface ICAM-1 followed a log-normal distribution. Median sICAM-1 concentrations increased with greater severity-of-illness: 279 ng/mL (UM, 462 ng/mL (SM-s, and 586 ng/mL (SM-f, p Conclusion In this cohort of children with P. falciparum malaria, sICAM-1 levels were associated with severity-of-illness. Patients with UM had higher monocyte ICAM-1 expression consistent with a role for monocyte ICAM-1 in immune clearance during non-severe malaria. Among the subsets of patients with either SMA or CM, monocyte ICAM-1 levels were higher in CM, consistent with the role of ICAM-1 as a marker of cytoadhesion. Categories of disease in pediatric malaria may exhibit specific combinations of soluble and cellular ICAM-1 expression.

  15. Soluble ICAM-1 serum levels in patients with intermediate uveitis

    OpenAIRE

    Klok, A.M.; Luyendijk, L.; Zaal, M.J.W.; Rothova, A; Kijlstra, A

    1999-01-01

    AIM—To investigate whether serum levels of soluble intercellular adhesion molecule 1 (sICAM-1) can serve as a marker of the presence of systemic disease in intermediate uveitis.
METHODS—In a multicentre study sICAM-1 serum levels were measured in 61 patients with idiopathic intermediate uveitis, controls included 56 uveitis patients with a systemic disease (26 sarcoid associated uveitis and 30 HLA-B27 positive acute anterior uveitis), 58 uveitis patients without systemic disease (30 toxoplasm...

  16. Overexpression of sICAM-1 in the Alveolar Epithelial Space Results in an Exaggerated Inflammatory Response and Early Death in Gram Negative Pneumonia

    Directory of Open Access Journals (Sweden)

    Curtis Jeffery L

    2011-01-01

    Full Text Available Abstract Background A sizeable body of data demonstrates that membrane ICAM-1 (mICAM-1 plays a significant role in host defense in a site-specific fashion. On the pulmonary vascular endothelium, mICAM-1 is necessary for normal leukocyte recruitment during acute inflammation. On alveolar epithelial cells (AECs, we have shown previously that the presence of normal mICAM-1 is essential for optimal alveolar macrophage (AM function. We have also shown that ICAM-1 is present in the alveolar space as a soluble protein that is likely produced through cleavage of mICAM-1. Soluble intercellular adhesion molecule-1 (sICAM-1 is abundantly present in the alveolar lining fluid of the normal lung and could be generated by proteolytic cleavage of mICAM-1, which is highly expressed on type I AECs. Although a growing body of data suggesting that intravascular sICAM-1 has functional effects, little is known about sICAM-1 in the alveolus. We hypothesized that sICAM-1 in the alveolar space modulates the innate immune response and alters the response to pulmonary infection. Methods Using the surfactant protein C (SPC promoter, we developed a transgenic mouse (SPC-sICAM-1 that constitutively overexpresses sICAM-1 in the distal lung, and compared the responses of wild-type and SPC-sICAM-1 mice following intranasal inoculation with K. pneumoniae. Results SPC-sICAM-1 mice demonstrated increased mortality and increased systemic dissemination of organisms compared with wild-type mice. We also found that inflammatory responses were significantly increased in SPC-sICAM-1 mice compared with wild-type mice but there were no difference in lung CFU between groups. Conclusions We conclude that alveolar sICAM-1 modulates pulmonary inflammation. Manipulating ICAM-1 interactions therapeutically may modulate the host response to Gram negative pulmonary infections.

  17. Gene expression of LOX-1, VCAM-1, and ICAM-1 in pre-atherosclerotic mice

    DEFF Research Database (Denmark)

    Fisker Hag, Anne Mette; Pedersen, Sune Folke; Kjaer, Andreas

    2008-01-01

    To identify markers of the earliest stage of atherosclerosis, endothelial dysfunction, we evaluated the gene expression of lectin-like oxidized-low-density-lipoprotein receptor-1 (LOX-1), vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) in very young pre......-atherosclerotic mice. Furthermore, the plasma levels of the soluble VCAM-1 and ICAM-1 were compared to the gene expression profiles. Gene expressions of LOX-1 and VCAM-1 were up-regulated in young apoE(-/-) mice, and thus, it seems probable that these genes play a role in pre-atherosclerosis. Contrarily, the gene...... expression profile of ICAM-1 did not show any apparent differences between the groups, questioning the involvement of this molecule in the early development of atherosclerosis. Plasma levels of sVCAM-1 and sICAM-1 were similar in all mice and did not correlate with the vascular gene expression...

  18. EXPRESSION OF ICAM-1 AND LFA-1 MOLECULES IN RELATION TO RENAL ALLOGRAFT REJECTION IN RATS

    Institute of Scientific and Technical Information of China (English)

    1999-01-01

    Objective.The purpose of this study was to assess the renal graft expression of ICAM-1(intercellular adhesion molecule-1) nd LFA-1(lymphocyte function-associated antigen-1)molecule with relation to graft rejection.Methods.Rat kiney transplantation was performed according to the procedure of Kamada with some modification.Experimental rats were divided into 5 groups.The survival time of recipient rats and function of grafts after renal transplantation were observed.The sections of renal graft were stained for monoclonal antibody ICAM-1 and LFA-1, and then quantification of ICAM-1 and LFA-1 expression was accomplished by computer image analysis.Results.ICAM-1 and LFA-1 increased significantly in the renal allograft rejection group as compared with the non-rejection groups(P<0.05).Conluson.Both biopsy of renal graft and monitoring of ICAM-1 and LFA-1 are useful tools in diagnosing and treating acute rejection.

  19. Targeting of ICAM-1 on vascular endothelium under static and shear stress conditions using a liposomal Gd-based MRI contrast agent

    NARCIS (Netherlands)

    Paulis, L.E.M.; Jacobs, I.; Akker, N. van de; Geelen, T.; Molin, D.; Starmans, L.W.; Nicolay, K.; Strijkers, G.J.

    2012-01-01

    ABSTRACT: BACKGROUND: The upregulation of intercellular adhesion molecule-1 (ICAM-1) on the endothelium of bloodvessels in response to pro-inflammatory stimuli is of major importance for the regulation oflocal inflammation in cardiovascular diseases such as atherosclerosis, myocardial infarctionand

  20. Effect of soluble ICAM-1 on a Sjögren's syndrome-like phenotype in NOD mice is disease stage dependent

    NARCIS (Netherlands)

    N. Roescher; J.L. Vosters; H. Yin; G.G. Illei; P.P. Tak; J.A. Chiorini

    2011-01-01

    Intercellular adhesion molecule-1 (ICAM-1) is involved in migration and co-stimulation of T and B cells. Membrane bound ICAM-1 is over expressed in the salivary glands (SG) of Sjögren's syndrome (SS) patients and has therefore been proposed as a potential therapeutic target. To test the utility of I

  1. The Expression of Integrin β3 and Intercellular Adhesion Molecule(ICAM-1)in Decidua and Chorionic Villi during Mifepristone Induced Abortion

    Institute of Scientific and Technical Information of China (English)

    李瑞珍; 王振海; 吴瑞芳

    1999-01-01

    The effects of mifepristone with misoprostol on the expression of the integrin β3 and intercellular adhesion motecule-1 (ICAM-1)in decidua and chorionic villi tissues in early pregnancy in 10 cases were investigated by immuno-ftow cytometry(the eyper-iment group).At the same time,the other 10 cases induced by mechanical vacuum as-piration were collected as the control.The results showed that,the positive rate of inte-grin β3 and ICAM-1 in decidua of the experiment group were 19.1±5. 01% and 20.61±6. 51%;while those in chorionic villi were 21.32±4. 38% and 20. 29±6. 49%,which were significantly lower than those in the control group.These results suggested that integrin β3 and ICAM-1 may take part in the maintenance of early pregnancy.The mechanism of mifepristone induced abortion may be mediated by the down-regulation of the integrin β3 and ICAM-1 expression in decidua and chorionic villi.

  2. Soluble Inter-Cellular Adhesion Molecule-1 in Urban Asian North Indians: Relationships with Anthropometric and Metabolic Covariates

    Directory of Open Access Journals (Sweden)

    Astha Sethi

    2002-01-01

    Full Text Available Background: High prevalence of diabetes, obesity, and dyslipidemias in people belonging to poor socio-economic strata in urban slums of northern India has been recorded recently. To assess whether this population has high levels of soluble intercellular adhesion molecule-1 (sICAM-1, a cytokine involved in the pathogenesis of atherosclerosis, we investigated subjects belonging to poor socio-economic strata in urban slums and compared them to healthy control subjects from non-slum urban areas of New Delhi.

  3. ICAM-1 Clustering on Endothelial Cells Recruits VCAM-1

    NARCIS (Netherlands)

    J.D. van Buul; J. van Rijssel; F.P.J. van Alphen; A.M. van Stalborch; E.P.J. Mul; P.L. Hordijk

    2010-01-01

    In the initial stages of transendothelial migration, leukocytes use the endothelial integrin ligands ICAM-1 and VCAM-1 for strong adhesion. Upon adhesion of the leukocyte to endothelial ICAM-1, ICAM-1 is clustered and recruited to the adhered leukocyte, promoting strong adhesion. In this study, we p

  4. Serum inter-cellular adhesion molecule 1 is an early marker of diagnosis and prediction of severe acute pancreatitis

    Institute of Scientific and Technical Information of China (English)

    Hai-Hang Zhu; Lin-Lin Jiang

    2012-01-01

    AIM:To determine if serum inter-cellular adhesion molecule 1 (ICAM-1) is an early marker of the diagnosis and prediction of severe acute pancreatitis (SAP)within 24 h of onset of pain,and to compare the sensitivity,specificity and prognostic value of this test with those of acute physiology and chronic health evaluation (APACHE) Ⅱ score and interleukin-6 (IL-6).METHODS:Patients with acute pancreatitis (AP) were divided into two groups according to the Ranson's criteria:mild acute pancreatitis (MAP) group and SAP group.Serum ICAM-1,APACHE Ⅱ and IL-6 levels were detected in all the patients.The sensitivity,specificity and prognostic value of the ICAM-1,APACHE Ⅱ score and IL-6 were evaluated.RESULTS:The ICAM-1 level in 36 patients with SAP within 24 h of onset of pain was increased and was significantly higher than that in the 50 patients with MAP and the 15 healthy volunteers (P < 0.01).The ICAM-1 level (25 ng/mL) was chosen as the optimum cutoff to distinguish SAP from MAP,and the sensitivity,specificity,positive predictive value,negative predictive value (NPV),positive likelihood ratio and negative likelihood ratio were 61.11%,71.42%,0.6111,0.7142,2.1382 and 0.5445,respectively.The area under the curve demonstrated that the prognostic accuracy of ICAM-1 (0.712) was similar to the APACHE-Ⅱ scoring system (0.770) and superior to IL-6 (0.508) in distinguishing SAP from MAP.CONCLUSION:ICAM-1 test is a simple,rapid and reliable method in clinical practice.It is an early marker of diagnosis and prediction of SAP within the first 24 h after onset of pain or on admission.As it has a relatively low NPV and does not allow it to be a stand-alone test for the diagnosis of AP,other conventional diagnostic tests are required.

  5. Involvement of MAPKs in ICAM-1 Expression in Glomerular Endothelial Cells in Diabetic Nephropathy

    Directory of Open Access Journals (Sweden)

    Watanabe,Naomi

    2011-08-01

    Full Text Available Inflammatory processes are involved in the pathogenesis of diabetic nephropathy. The aim of this study was to clarify the role of mitogen-activated protein kinase (MAPK pathways for induction of intercellular adhesion molecule-1 (ICAM-1 expression in glomerular endothelial cells under diabetic conditions. We examined the expression of ICAM-1 in the kidneys of experimental diabetic rats. Human glomerular endothelial cells (GE cells were exposed to normal glucose concentration, high glucose concentration (HG, or high mannitol concentration (HM, and then the expression of the ICAM-1 protein and the phosphorylation of the 3 subfamilies of mitogen-activated protein kinase (MAPK were determined using Western blot analysis. Next, to evaluate the involvement of MAPKs in HG- or HM-induced ICAM-1 expression, we preincubated GE cells with the inhibitors for ERK, p38 or JNK 1h prior to the application of glucose or mannitol. Expression of ICAM-1 was increased in the glomeruli of diabetic rats. Both HG and HM induced ICAM-1 expression and phosphorylation of ERK1/2, p38 and JNK in GE cells. Expression of ICAM-1 was significantly attenuated by inhibitors of ERK, p38 and JNK. We conclude that activation of ERK1/2, p38 and JNK cascades may be involved in ICAM-1 expression in glomerular endothelial cells under diabetic conditions.

  6. Increased plasma concentrations of sICAM-1, sVCAM-1 and sELAM-1 in patients with Plasmodium falciparum or em>P. vivax malaria and association with disease severity

    DEFF Research Database (Denmark)

    Jakobsen, P H; Morris-Jones, S; Rønn, A;

    1994-01-01

    Increased serum concentrations of soluble intercellular adhesion molecule-1 (sICAM-1), soluble endothelial leucocyte adhesion molecule-1 (sELAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) were detected in Danish malaria patients infected with sequestering Plasmodium falciparum or n...

  7. Activation of transcription factor AP-2 mediates UVA radiation- and singlet oxygen-induced expression of the human intercellular adhesion molecule 1 gene

    Energy Technology Data Exchange (ETDEWEB)

    Grether-Beck, S.; Olaizola-Horn, S.; Schmitt, H.; Grewe, M. [Clinical and Experimental Photodermatology, Duesseldorf (Germany)] [and others

    1996-12-10

    UVA radiation is the major component of the UV solar spectrum that reaches the earth, and the therapeutic application of UVA radiation is increasing in medicine. Analysis of the cellular effects of UVA radiation has revealed that exposure of human cells to UVA radiation at physiological doses leads to increased gene expression and that this UVA response is primarily mediated through the generation of singlet oxygen. In this study, the mechanisms by which UVA radiation induces transcriptional activation of the human intercellular adhesion molecule 1 (ICAM-1) were examined. UVA radiation was capable of inducing activation of the human ICAM-1 promoter and increasing OCAM-1 mRNA and protein expression. These UVA radiation effects were inhibited by singlet oxygen quenchers, augmented by enhancement of singlet oxygen life-time, and mimicked in unirradiated cells by a singlet oxygen-generating system. UVA radiation as well as singlet oxygen-induced ICAM-1 promoter activation required activation of the transcription factor AP-2. Accordingly, both stimuli activated AP-2, and deletion of the putative AP-2-binding site abrogated ICAM-1 promoter activation in this system. This study identified the AP-2 site as the UVA radiation- and singlet oxygen-responsive element of the human ICAM-1 gene. The capacity of UVA radiation and/or singlet oxygen to induce human gene expression through activation of AP-2 indicates a previously unrecognized role of this transcription factor in the mammalian stress response. 38 refs., 3 figs., 3 tabs.

  8. Maternal serum uric acid concentration is associated with the expression of tumour necrosis factor-α and intercellular adhesion molecule-1 in patients with preeclampsia.

    Science.gov (United States)

    Zhao, J; Zheng, D-Y; Yang, J-M; Wang, M; Zhang, X-T; Sun, L; Yun, X-G

    2016-07-01

    We aimed to investigate whether there is a correlation between elevated serum uric acid (SUA) concentration and endothelial inflammatory response in women with preeclampsia (PE). On the basis of clinical and laboratory findings, patients were assigned to three groups: normal blood pressure (Control (Con)), gestational hypertension (GH) and PE (n=50 in each group). SUA concentration was measured by spectrophotometry, and serum tumour necrosis factor-α (TNF-α) and intercellular adhesion molecule-1 (ICAM-1) levels were measured by enzyme-linked immunosorbent assay. Western blotting and immunohistochemical staining were also used to detect the changes in TNF-α and ICAM-1 expression in subcutaneous fat tissue. PE patients showed significantly higher systolic and diastolic blood pressures compared with Con and GH pregnant women (P=0.02 and P=0.02, respectively). The changes of body mass index (ΔBMI) before and after pregnancy and 24-h urine protein were significantly different among the three groups (P<0.001). Maternal SUA, TNF-α and soluble ICAM-1 (sICAM-1) levels were significantly increased in the patients with PE (P<0.05) compared with the other two groups. Scatterplot analysis revealed that elevated SUA concentration positively correlated with TNF-α and sICAM-1 in pregnant women. Moreover, vessels in subcutaneous fat tissues of preeclamptic patients showed intense TNF-α and ICAM-1 staining compared with Con and GH patients. The results support that, to a certain extent, elevated SUA concentration is significantly associated with inflammation of maternal systemic vasculature as indicated by increased TNF-α and ICAM-1 expression in women with PE. PMID:26511169

  9. The Value of the Soluable Intercellular Adhesion Molecule-1 Levelsin Matermal Serum for Determination of Occult Chorioamnionitis in Premature Rupture of Membranes

    Institute of Scientific and Technical Information of China (English)

    邹丽; 张会军; 祝建芳; 朱剑文

    2004-01-01

    To compare the diagnostic value of soluble intercellular adhesion molecule 1 (sICAM-1)with that of c-reactive protein (CRP) for detecting chorioamnionitis (CAM) in serum of women with premature rupture of membranes (PROM), 55 pregnant women with PROM, including 18pregnant women with preterm premature rupture of membranes (PPROM) and 20 normal pregnant women at term (TPROM) were studied. Maternal serum were measured by Sandwish enzymelinked immunoabsorbent assay (ELISA) for sICAM. CAM was histologically confirmed after delivery. The results revealed that (1) maternal serum levels of sICAM-1 and CRP were significantly higher in women with PROM than those without it; (2) maternal serum levels of sICAM-1 and CRP were significantly higher in women with CAM than those without it; (3) serum levels of sICAM-1 in PPROM women were similar to those in TPROM women, whereas serum levels of CRP in PPROM women were significantly higher than those in TPROM women; (4) the sensitivity,specificity, positive predictive value, negative predictive value, Kappa index and area under receiver operating characteristic (ROC) curve of maternal serum sICAM-1 (cutoff 104.7 ng/ml) and CRP (cutoff 1.03 mg/dl) for diagnosing CAM were 100 %, 91.2 %, 87.5 %, 100 %, 0.20, 0.995and 81.0 %, 73.5 %, 65.4 %, 86.2 %, 0.13, 0. 811, respectively; (5) among the mild histological CAM group, severe histological CAM group and clinical CAM group, the difference in maternal serum levels of sICAM-1 were significantly (P<0. 001), with the order of concentration from high level to low level corresponding to the severity of CAM. It is concluded that maternal serum level of ICAM-1 is superior to that of CRP as biomarker for diagnosing intraamniotic infection in pregnant women with PROM.

  10. P-selectin/ICAM-1 double mutant mice: acute emigration of neutrophils into the peritoneum is completely absent but is normal into pulmonary alveoli.

    OpenAIRE

    Bullard, D C; Qin, L.; Lorenzo, I.; Quinlin, W M; Doyle, N A; Bosse, R; Vestweber, D; Doerschuk, C. M.; Beaudet, A L

    1995-01-01

    Neutrophil emigration during an inflammatory response is mediated through interactions between adhesion molecules on endothelial cells and neutrophils. P-Selectin mediates rolling or slowing of neutrophils, while intercellular adhesion molecule-1 (ICAM-1) contributes to the firm adhesion and emigration of neutrophils. Removing the function of either molecule partially prevents neutrophil emigration. To analyze further the role of P-selectin and ICAM-1, we have generated a line of mice with mu...

  11. 可溶性细胞间粘附分子-1在新生儿缺氧缺血性脑病血清的表达及意义%Expression and significance of soluble intercellular adhesion molecule-1 in newborn’s serum with neonatal hypoxic ischemic encephalopathy

    Institute of Scientific and Technical Information of China (English)

    王彦彦; 张莹; 田淑霞

    2015-01-01

    目的:研究可溶性细胞间粘附分子-1(ICAM-1)在新生儿缺氧缺血性脑病(HIE)患儿血清中的表达及意义,探讨可溶性ICAM-1与新生儿缺氧缺血性脑病病情严重程度的关系。方法采用酶联免疫双抗体夹心法(ELISA)检测HIE新生儿和健康新生儿血清中可溶性ICAM-1的表达,将可溶性ICAM-1的表达量与HIE的严重程度之间进行相关性分析。结果 HIE血清可溶性ICAM-1的水平均高于对照组,在HIE各组血清中可溶性ICAM-1的浓度为重度>中度>轻度,HIE患儿血清可溶性ICAM-1表达与临床分度呈正相关。结论可溶性ICAM-1在HIE血清中呈高表达,可溶性ICAM-1的表达与病情严重程度密切相关,可溶性ICAM-1在HIE中起着重要作用,可能提示HIE早期分子生物学变化。%ABSTRACT:Objective To investigate expression and significance of soluble intercellular adhesion molecule-1 (ICAM-1) in newborn’s serum with neonatal hypoxic ischemic encephalopathy, and investigate relationship between soluble ICAM-1 and severity of neonatal hypoxic ischemic encephalopathy. Method examine expression of soluble ICAM-1 in serum of HIE and healthy newborns by enzyme linked immunosorbent assay (ELISA), and analyze correlation between expression amount of soluble ICAM-1 and severity of HIE. Result soluble ICAM-1 level in HIE serum was higher than that of control group. And concentration of soluble ICAM-1 in each group HIE serum shows Severe>Moderate>Mild. Serum soluble ICAM-1 expression of HIE newborns were positively correlated with clinical grading. Conclusion soluble ICAM-1 in HIE serum shows high expression, soluble ICAM-1 expression is closely related to disease severity, and soluble ICAM-1 plays important role in HIE, which may suggest early molecular changes of HIE.

  12. Changes in the vascular cell adhesion molecule-1, intercellular adhesion molecule-1 and c-reactive protein following administration of aqueous extract of piper sarmentosum on experimental rabbits fed with cholesterol diet

    Directory of Open Access Journals (Sweden)

    Al-Mekhlafi Hesham M

    2011-01-01

    Full Text Available Abstract Background Inflammation process plays an important role in the development of atherosclerosis. Hypercholesterolemia is one of the major risk factors for atherosclerosis. The present study aimed to evaluate the effect of aqueous extract of Piper sarmentosum (P.s on inflammatory markers like vascular cell adhesion molecule-1 (VCAM-1, intercellular adhesion molecule-1 (ICAM-1, and C-reactive protein (CRP. Methods Forty two male New Zealand white rabbits were divided equally into seven groups; (i C- control group fed normal rabbit chow (ii CH- cholesterol diet (1%cholesterol (iii X1- 1% cholesterol with water extract of P.s (62.5 mg/kg (iv X2- 1% cholesterol with water extract of P.s (125 mg/kg (v X3- 1% cholesterol with water extract of P.s (250 mg/kg (vi X4- 1% cholesterol with water extract of P.s (500 mg/kg and (vii SMV group fed with 1% cholesterol supplemented with simvistatin drug (1.2 mg/kg. All animals were treated for 10 weeks. Blood serum was taken for observing the inflammatory markers at the beginning and end of the experiment. Results Rabbits fed with 1% cholesterol diet (CH showed significant increase in the level of VCAM-1, ICAM-1 and CRP compared to the C group. The levels of VCAM-1, ICAM-1 and CRP in the 1% cholesterol group and supplemented with P.s (500 mg/kg were significantly reduced compared to the cholesterol group. Similar results were also reported with simvistatin group. Conclusion These results suggest that the supplementation of Piper sarmentosum extract could inhibit inflammatory markers which in turn could prevent atherosclerosis.

  13. Neutrophil Interactions with Epithelial Expressed ICAM-1 Enhances Intestinal Mucosal Wound Healing

    Science.gov (United States)

    Sumagin, R; Brazil, JC; Nava, P; Nishio, H; Alam, A; Luissint, AC; Weber, DA; Neish, AS; Nusrat, A; Parkos, CA

    2015-01-01

    A characteristic feature of gastrointestinal tract inflammatory disorders, such as inflammatory bowel disease, is polymorphonuclear neutrophil (PMN) transepithelial migration (TEM) and accumulation in the gut lumen. PMN accumulation within the intestinal mucosa contributes to tissue injury. While epithelial infiltration by large numbers of PMNs results in mucosal injury, we found that PMN interactions with luminal epithelial membrane receptors may also play a role in wound healing. Intercellular adhesion molecule-1 (ICAM-1) is a PMN ligand that is upregulated on apical surfaces of intestinal epithelial cells under inflammatory conditions. In our study, increased expression of ICAM-1 resulted in enhanced PMN binding to the apical epithelium, which was associated with reduced PMN apoptosis. Following TEM, PMN adhesion to ICAM-1 resulted in activation of Akt and β-catenin signaling, increased epithelial-cell proliferation, and wound healing. Such responses were ICAM-1 dependent as engagement of epithelial ICAM-1 by antibody-mediated cross-linking yielded similar results. Furthermore, using an in-vivo biopsy-based, colonic-mucosal-injury model, we demonstrated epithelial ICAM-1 plays an important role in activation of epithelial Akt and β-catenin signaling and wound healing. These findings suggest that post-migrated PMNs within the intestinal lumen can regulate epithelial homeostasis, thereby identifying ICAM-1 as a potential therapeutic target for promoting mucosal wound healing. PMID:26732677

  14. Expression of Cell Adhesion Molecule ICAM-1 in Leukocytes of Chronic Periodontitis Affected Gingiva%细胞粘附ICAM-1慢性牙周炎牙龈组织中白细胞的表达

    Institute of Scientific and Technical Information of China (English)

    闫萍; 乐进秋; 江汉

    2003-01-01

    目的研究ICAM-1在慢性牙周炎牙龈组织中白细胞的表达,探讨ICAM-1在慢性牙周炎免疫病因机理中和作用.方法应用抗ICAM-1单克隆抗体,通过碱性磷酸酶-抗碱性磷酸酶的免疫组织化学技术,对ICAM-1在正常和慢性牙周炎的牙龈组织中白细胞的表达进行分析.结果 ICAM-1阳性白细胞主要聚集于慢性牙周炎结合上皮和袋上皮下方结缔组织中,慢性牙周炎牙龈组织单位面积中表达ICAM-1阳性的白细胞的比例显著高于正常牙龈组(P<0.01).结论 ICAM-1可能参与和调节慢性牙周炎牙龈组织中白细胞介导的免疫粘附过程.

  15. Arginase levels and their association with Th17-related cytokines, soluble adhesion molecules (sICAM-1 and sVCAM-1) and hemolysis markers among steady-state sickle cell anemia patients

    Science.gov (United States)

    Vilas-Boas, Wendell; Cerqueira, Bruno A. V.; Zanette, Angela M. D.; Reis, Mitermayer G.; Barral-Netto, Manoel

    2010-01-01

    Sickle cell anemia (SCA) is characterized by a marked endothelial dysfunction, owing to many factors. Arginine metabolism can be related to the inflammatory chronic state presented by patients, playing a key role in their clinical outcome and vascular endothelium. We investigated the serum arginase levels in 50 SCA patients (22 men and 28 women, mean age of 17 ± 10.5 years) and 28 healthy controls. Serum arginase levels were associated with biochemical hemolysis markers and cytokines involved in Th17 response, as well as levels of soluble intercellular adhesion molecule-1 (sICAM-1) and vascular cell adhesion molecule-1 (sVCAM-1). Arginase concentrations were higher in SCA patients, compared with controls (p = 0.005), and were significantly and positively associated with total bilirubin (p = 0.004), indirect bilirubin (p = 0.04), and aspartate aminotransferase (AST; p = 0.039) in the SCA patient group. Moreover, arginase was significantly and positively associated with transforming growth factor-beta (TGF-beta; p = 0.008) among SCA patients. sICAM-1 was significantly and positively associated to reticulocytes (p = 0.014) and AST (p = 0.04). sVCAM-1 was likewise associated with lactate dehydrogenase (p = 0.03). These data suggest a new insight into arginase metabolism, as we show here a shift in arginine catabolism, where TGF-beta may induces the arginase pathway instead of the nitric oxide pathway and a possible involvement of the vascular activation and the serum arginase in chronic hemolysis among SCA patients. Additional studies should be carried out in order to investigate the mechanisms by which TGF-beta participates in the metabolism of arginase in SCA patients. PMID:20405289

  16. Regional gene expression of LOX-1, VCAM-1, and ICAM-1 in aorta of HIV-1 transgenic rats

    DEFF Research Database (Denmark)

    Hag, Anne Mette Fisker; Kristoffersen, Ulrik Sloth; Pedersen, Sune Folke;

    2009-01-01

    endpoints, studies in animal models could be attractive alternatives. METHODOLOGY/PRINCIPAL FINDINGS: We evaluated gene expression of lectin-like oxidized-low-density-lipoprotein receptor-1 (LOX-1), vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) in HIV-1...... transgenic (HIV-1Tg) rats; these genes are all thought to play important roles in early atherogenesis. Furthermore, the plasma level of sICAM-1 was measured. We found that gene expressions of LOX-1 and VCAM-1 were higher in the aortic arch of HIV-1Tg rats compared to controls. Also, the level of sICAM-1...... was elevated in the HIV-1Tg rats compared to controls, but the ICAM-1 gene expression profile did not show any differences between the groups. CONCLUSIONS/SIGNIFICANCE: HIV-1Tg rats have gene expression patterns indicating endothelial dysfunction and accelerated atherosclerosis in aorta, suggesting that HIV...

  17. Polymorphism K469E of intercellular adhesion molecule-1 gene and restenosis after coronary stenting in Chinese patients

    Institute of Scientific and Technical Information of China (English)

    刘兆平; 霍勇; 李建平; 张岩; 薛琳; 赵春玉; 洪秀梅; 黄爱群; 高炜

    2004-01-01

    Background Inflammation is a major cause of restenosis after coronary stenting. Intercellular adhesion molecule-1 ( ICAM-1 ) is an important adhesion molecule that plays a key role in the tight adhesion between leukocytes and vascular endothelium. The object of this study was to investigate the association between the K469E polymorphism of the ICAM-1 gene and restenosis after coronary stenting in North Chinese population.Methods The ICAM-1 K469E polymorphism was genotyped using polymerase chain reaction- restriction fragment length polymorphism method in 124 patients who had undergone coronary stenting and coronary angiography at least 3 months earlier. Information on clinical risk factors and procedure- related data were also collected. Results Of 124 enrolled patients in total, there were 72 cases of in-stent restenosis. The restenosis rate in this population was 58. 1%. The frequencies of the three possible genotypes of the ICAM-1 K469E polymorphism were: KK genotype 50.8%, EE genotype 41.9%, and EK genotype 41.9%.Among restenosis patients, the frequency of the KK genotype was 58. 3% and the frequency of E allele carriers was 41.7%. Among non-restenosis patients, the frequency of the KK genotype was 40.4%, and the frequency of E allele carriers was 59. 6%. The distribution of these two genotype groups between restenosis and non-restenosis patients was significantly different (P=0.049). Using multivariate logistic regression, the difference between the two groups was more apparent. The odds ratio of KK homozygotes vs E allele carriers was 2.6, with 95% confidence interval 1.2 -5.8 (P =0. 018). After grading of risk factors, we found that the KK genotype was a stronger predictor of in- stent restenosis in obesity or hyperlipemia patients, with an odds ratio of 9.3 and 3.7, respectively (P<0.05).Conclusion In our study population, KK homozygotes of the ICAM-1 codon 469 mutation had a higher risk of restenosis after coronary stenting, especially in the case of obese

  18. Activated endothelial interleukin-1beta, -6, and -8 concentrations and intercellular adhesion molecule-1 expression are attenuated by lidocaine.

    LENUS (Irish Health Repository)

    Lan, Wei

    2012-02-03

    Endothelial cells play a key role in ischemia reperfusion injury. We investigated the effects of lidocaine on activated human umbilical vein endothelial cell (HUVEC) interleukin (IL)-1beta, IL-6, and IL-8 concentrations and intercellular adhesion molecule-1 (ICAM-1) expression. HUVECs were pretreated with different concentrations of lidocaine (0 to 0.5 mg\\/mL) for 60 min, thereafter tumor necrosis factor-alpha was added at a concentration of 2.5 ng\\/mL and the cells incubated for 4 h. Supernatants were harvested, and cytokine concentrations were analyzed by enzyme-linked immunosorbent assay. Endothelial ICAM-1 expression was analyzed by using flow cytometry. Differences were assessed using analysis of variance and post hoc unpaired Student\\'s t-test where appropriate. Lidocaine (0.5 mg\\/mL) decreased IL-1beta (1.89 +\\/- 0.11 versus 4.16 +\\/- 1.27 pg\\/mL; P = 0.009), IL-6 (65.5 +\\/- 5.14 versus 162 +\\/- 11.5 pg\\/mL; P < 0.001), and IL-8 (3869 +\\/- 785 versus 14,961 +\\/- 406 pg\\/mL; P < 0.001) concentrations compared with the control. IL-1beta, IL-6, and IL-8 concentrations in HUVECs treated with clinically relevant plasma concentrations of lidocaine (0.005 mg\\/mL) were similar to control. ICAM-1 expression on lidocaine-treated (0.05 mg\\/mL) HUVECs was less than on controls (198 +\\/- 52.7 versus 298 +\\/- 50.3; Mean Channel Fluorescence; P < 0.001). Activated endothelial IL-1beta, IL-6, and IL-8 concentrations and ICAM-1 expression are attenuated only by lidocaine at concentrations larger than clinically relevant concentrations.

  19. ICAM-1 is necessary for epithelial recruitment of gammadelta T cells and efficient corneal wound healing.

    Science.gov (United States)

    Wound healing and inflammation are both significantly reduced in mice that lack gammadelta T cells. Here, the role of epithelial intercellular adhesion molecule-1 (ICAM-1) in gammadelta T cell migration in corneal wound healing was assessed. Wild-type mice had an approximate fivefold increase in epi...

  20. Breast cancer cells compete with hematopoietic stem and progenitor cells for intercellular adhesion molecule 1-mediated binding to the bone marrow microenvironment.

    Science.gov (United States)

    Dhawan, Abhishek; Friedrichs, Jens; Bonin, Malte von; Bejestani, Elham Peshali; Werner, Carsten; Wobus, Manja; Chavakis, Triantafyllos; Bornhäuser, Martin

    2016-08-01

    Adhesion-based cellular interactions involved in breast cancer metastasis to the bone marrow remain elusive. We identified that breast cancer cells directly compete with hematopoietic stem and progenitor cells (HSPCs) for retention in the bone marrow microenvironment. To this end, we established two models of competitive cell adhesion-simultaneous and sequential-to study a potential competition for homing to the niche and displacement of the endogenous HSPCs upon invasion by tumor cells. In both models, breast cancer cells but not non-tumorigenic cells competitively reduced adhesion of HSPCs to bone marrow-derived mesenchymal stromal cells (MSCs) in a tumor cell number-dependent manner. Higher adhesive force between breast cancer cells and MSCs, as compared with HSPCs, assessed by quantitative atomic force microscopy-based single-cell force spectroscopy could partially account for tumor cell mediated reduction in HSPC adhesion to MSCs. Genetic inactivation and blockade studies revealed that homophilic interactions between intercellular adhesion molecule 1 (ICAM-1) expressed on tumor cells and MSCs, respectively, regulate the competition between tumor cells and HSPCs for binding to MSCs. Moreover, tumor cell-secreted soluble ICAM-1(sICAM-1) also impaired HSPC adhesion via blocking CD18-ICAM-1 binding between HSPCs and MSCs. Xenotransplantation studies in NOD.Cg-Prkdc(scid) Il2rg(tm1Wjl)/SzJ mice revealed reduction of human HSPCs in the bone marrow via metastatic breast cancer cells. These findings point to a direct competitive interaction between disseminated breast cancer cells and HSPCs within the bone marrow micro environment. This interaction might also have implications on niche-based tumor support. Therefore, targeting this cross talk may represent a novel therapeutic strategy. PMID:27207667

  1. The Crystal Structure of Coxsackievirus A21 and Its Interaction with ICAM-1

    Energy Technology Data Exchange (ETDEWEB)

    Xiao, Chuan; Bator-Kelly, Carol M.; Rieder, Elizabeth; Chipman, Paul R.; Craig, Alister; Kuhn, Richard J.; Wimmer, Eckard; Rossmann, Michael G. (Liverpool); (SBU); (Purdue)

    2010-11-30

    CVA21 and polioviruses both belong to the Enterovirus genus in the family of Picornaviridae, whereas rhinoviruses form a distinct picornavirus genus. Nevertheless, CVA21 and the major group of human rhinoviruses recognize intercellular adhesion molecule-1 (ICAM-1) as their cellular receptor, whereas polioviruses use poliovirus receptor. The crystal structure of CVA21 has been determined to 3.2 {angstrom} resolution. Its structure has greater similarity to poliovirus structures than to other known picornavirus structures. Cryo-electron microscopy (cryo-EM) was used to determine an 8.0 {angstrom} resolution structure of CVA21 complexed with an ICAM-1 variant, ICAM-1{sup Kilifi}. The cryo-EM map was fitted with the crystal structures of ICAM-1 and CVA21. Significant differences in the structure of CVA21 with respect to the poliovirus structures account for the inability of ICAM-1 to bind polioviruses. The interface between CVA21 and ICAM-1 has shape and electrostatic complementarity with many residues being conserved among those CVAs that bind ICAM-1.

  2. There is no association between K469E ICAM-1 gene polymorphism and biliary atresia

    Institute of Scientific and Technical Information of China (English)

    Paisarn Vejchapipat; Naruemol Jirapanakom; Nutchanart Thawornsuk; Apiradee Theamboonlers; Voranush Chongsrisawat; Soottiporn Chittmittrapap; Yong Poovorawan

    2005-01-01

    AIM: To determine whether there was an association between inter-cellular adhesion molecule-1 (ICAM-1) gene polymorphism and biliary atresia (BA), and to investigate the relationship between serum soluble ICAM-1 (sICAM-1)and clinical outcome in BA patients after surgical treatment.METHODS: Eighty-three BA patients and 115 normal controls were genotyped. K469EICAM-1 polymorphism was analyzed using PCR assay. Serum sICAM-1 was determined using ELISA method from 72 BA patients. In order to evaluate the association between these variables and their clinical outcome, the patients were categorized into two groups:patients without jaundice and those with persistent jaundice.RESULTS: There were no significant differences between BA patients and controls in terms of gender, K469E ICAM-1genotypes, and alleles. The proportion of patients having serum sICAM-1 ≥3 500 ng/mL in persistent jaundice group was significantly higher than that in the other group. In addition, there was no association between K469EICAM-1polymorphism and the status of jaundice in BA patients after Kasai operation.CONCLUSION: ICAM-1 possibly plays an important and active role in the disease progression. However, the process is not associated with genetic variation of K469EICAM-1 polymorphism.

  3. ICAM1 Is a Potential Cancer Stem Cell Marker of Esophageal Squamous Cell Carcinoma.

    Directory of Open Access Journals (Sweden)

    Sheng-Ta Tsai

    Full Text Available Esophageal squamous cell carcinoma (ESCC accounts for about 90% of esophageal cancer diagnosed in Asian countries, with its incidence on the rise. Cancer stem cell (CSC; also known as tumor-initiating cells, TIC is inherently resistant to cytotoxic chemotherapy and radiation and associates with poor prognosis and therapy failure. Targeting therapy against cancer stem cell has emerged as a potential therapeutic approach to develop effective regimens. However, the suitable CSC marker of ESCC for identification and targeting is still limited. In this study, we screened the novel CSC membrane protein markers using two distinct stemness characteristics of cancer cell lines by a comparative approach. After the validation of RT-PCR, qPCR and western blot analyses, intercellular adhesion molecule 1 (ICAM1 was identified as a potential CSC marker of ESCC. ICAM1 promotes cancer cell migration, invasion as well as increasing mesenchymal marker expression and attenuating epithelial marker expression. In addition, ICAM1 contributes to CSC properties, including sphere formation, drug resistance, and tumorigenesis in mouse xenotransplantation model. Based on the analysis of ICAM1-regulated proteins, we speculated that ICAM1 regulates CSC properties partly through an ICAM1-PTTG1IP-p53-DNMT1 pathway. Moreover, we observed that ICAM1 and CD44 could have a compensation effect on maintaining the stemness characteristics of ESCC, suggesting that the combination of multi-targeting therapies should be under serious consideration to acquire a more potent therapeutic effect on CSC of ESCC.

  4. Decreased pulmonary inflammation after ethanol exposure and burn injury in intercellular adhesion molecule-1 knockout mice.

    Science.gov (United States)

    Bird, Melanie D; Morgan, Michelle O; Ramirez, Luis; Yong, Sherri; Kovacs, Elizabeth J

    2010-01-01

    Clinical and laboratory evidence suggests that alcohol consumption dysregulates immune function. Burn patients who consume alcohol before their injuries demonstrate higher rates of morbidity and mortality, including acute respiratory distress syndrome, than patients without alcohol at the time of injury. Our laboratory observed higher levels of proinflammatory cytokines and leukocyte infiltration in the lungs of mice after ethanol exposure and burn injury than with either insult alone. To understand the mechanism of the increased pulmonary inflammatory response in mice treated with ethanol and burn injury, we investigated the role of intercellular adhesion molecule (ICAM)-1. Wild-type and ICAM-1 knockout (KO) mice were treated with vehicle or ethanol and subsequently given a sham or burn injury. Twenty-four hours postinjury, lungs were harvested and analyzed for indices of inflammation. Higher numbers of neutrophils were observed in the lungs of wild-type mice after burn and burn with ethanol treatment. This increase in pulmonary inflammatory cell accumulation was significantly lower in the KO mice. In addition, levels of KC, interleukin-1beta, and interleukin-6 in the lung were decreased in the ICAM-1 KO mice after ethanol exposure and burn injury. Interestingly, no differences were observed in serum or lung tissue content of soluble ICAM-1 24 hours postinjury. These data suggest that upregulation of adhesion molecules such as ICAM-1 on the vascular endothelium may play a critical role in the excessive inflammation seen after ethanol exposure and burn injury.

  5. Role of ICAM-1 polymorphisms (G241R, K469E) in mediating its single-molecule binding ability: Atomic force microscopy measurements on living cells

    Energy Technology Data Exchange (ETDEWEB)

    Bai, Rui [Chinese (301) General Hospital, 28 Fuxing Road, Haidian District, Beijing 100853 (China); Yi, Shaoqiong [Beijing Institute of Biotechnology, 20 Dongdajie, Fengtai, Beijing 100071 (China); Zhang, Xuejie [Beijing National Laboratory for Molecular Sciences, Key Laboratory of Molecular Nanostructure and Nanotechnology, Institute of Chemistry Chinese Academy of Sciences, 2 Zhongguancun North 1st Street, Beijing 100190 (China); Liu, Huiliang, E-mail: lhl518@vip.sina.com [Department of Cardiology, The General Hospital of Chinese People’s Armed Police Forces, Beijing 100039 (China); Fang, Xiaohong, E-mail: xfang@iccas.ac.cn [Beijing National Laboratory for Molecular Sciences, Key Laboratory of Molecular Nanostructure and Nanotechnology, Institute of Chemistry Chinese Academy of Sciences, 2 Zhongguancun North 1st Street, Beijing 100190 (China)

    2014-06-13

    Highlights: • We evaluated both single molecule binding ability and expression level of 4 ICAM-1 mutations. • AFM was used to measure single-molecule binding ability on living cells. • The SNP of ICAM-1 may induce changes in expressions rather than single-molecule binding ability. - Abstract: Atherosclerosis (As) is characterized by chronic inflammation and is a major cause of human mortality. ICAM-1-mediated adhesion of leukocytes in vessel walls plays an important role in the pathogenesis of atherosclerosis. Two single nucleotide polymorphisms (SNPs) of human intercellular adhesion molecule-1 (ICAM-1), G241R and K469E, are associated with a number of inflammatory diseases. SNP induced changes in ICAM-1 function rely not only on the expression level but also on the single-molecule binding ability which may be affected by single molecule conformation variations such as protein splicing and folding. Previous studies have shown associations between G241R/K469E polymorphisms and ICAM-1 gene expression. Nevertheless, few studies have been done that focus on the single-molecule forces of the above SNPs and their ligands. In the current study, we evaluated both single molecule binding ability and expression level of 4 ICAM-1 mutations – GK (G241/K469), GE (G241/E469), RK (R241/K469) and RE (R241/E469). No difference in adhesion ability was observed via cell adhesion assay or atomic force microscopy (AFM) measurement when comparing the GK, GE, RK, or RE genotypes of ICAM-1 to each other. On the other hand, flow cytometry suggested that there was significantly higher expression of GE genotype of ICAM-1 on transfected CHO cells. Thus, we concluded that genetic susceptibility to diseases related to ICAM-1 polymorphisms, G241R or K469E, might be due to the different expressions of ICAM-1 variants rather than to the single-molecule binding ability of ICAM-1.

  6. Labeling intercellular adhesion molecule 1 with 125I and the identification of its purity and immune activity%细胞间粘附分子-1125I标记及其纯度、免疫活性的鉴定

    Institute of Scientific and Technical Information of China (English)

    张志友; 方佩华; 侯秉璋; 高硕; 吕枚

    2001-01-01

    目的:建立细胞间粘附分子-1(intracellular adhesion molecule-1 ICAM-1)125I标记方法及鉴定其纯度和免疫活性.方法:用氯胺-T法标记ICAM-1,用Sephadex G-50柱层析分离,用纸层析法鉴定125I-ICAM-1的纯度,放免法检测其免疫活性.结果:125I-ICAM-1比活度为77 84μCi/μg蛋白,标记率为65.54%,125I-Na的放化纯度为97.27%,125I-ICAM-1能够与ICAM-1-Ab的最大结合为88.64%,并且随ICAM-1-Ab滴度的降低而增高.结论:成功建立125I标记ICAM-1的方法,并且125I-ICAM-1具有一定的免疫活性.

  7. Polymorphisms and linkage analysis for ICAM-1 and the selectin gene cluster

    Energy Technology Data Exchange (ETDEWEB)

    Vora, D.K.; Rosenbloom, C.L.; Cottingham, R.W. [Baylor College of Medicine, Houston, TX (United States)] [and others

    1994-06-01

    Genetic polymorphisms in leukocyte and endothelial cell adhesion molecules may be important variables with regard to susceptibility to multifactorial disease processes that include an inflammatory component. For this reason, polymorphisms were sought for intercellular adhesion molecule-1 (ICAM-1; gene symbol ICAM1) and for the three genes in the selectin cluster, P-selectin, L-selectin, and E-selectin (gene symbols SELP, SELL, and SELE, respectively). Two amino acid polymorphisms were identified for ICAM-1; Gly or Arg at codon 241 and Lys or Glu at codon 469. Dinucleotide repeat polymorphisms were identified in the 3{prime}-untranslated region for ICAM-1 and in intron 9 for P-selectin. Restriction fragment length polymorphisms were found using cDNAs for each of the three selectin genes as probes; E-selectin with BglII, P-selectin with ScaI, and L-selectin with HincII. Linkage analysis was performed for the selectin gene cluster and for ICAM-1 using the CEPH families; ICAM-1 is very tightly linked to the LDL receptor on chromosome 19, and the selectin cluster is linked to markers at chromosome 1q23. 41 refs., 2 tabs.

  8. IFN-γ诱导HaCaT细胞ICAM-1表达的条件优化%Optimizing on IFN - γ- induced ICAM - 1 Expression in HaCaT Cells

    Institute of Scientific and Technical Information of China (English)

    伍春莲

    2011-01-01

    Intercellular adhesion molecule - 1 ( ICAM - 1 ) was necessary for leukocyte and kerationocyte interaction.Upregulation of ICAM - 1 expression in keratinocytes had correlation with many skin inflammation.The purpose of this study was to optimize conditions of IFN - γ- induced ICAM - 1 expression on HaCaT cells in vitro.HaCaT cells were stimulated by IFN -γ at different concentration and time respectively.IFN -γ -induced ICAM -1 expression was detected in HaCaT cells by flow cytometry.Finally treatment of HaCaT cells with 1000U/mL IFN - γfor 24h markedly induced ICAM - 1 expression.The results indicated that IFN - γcould up-regulate.The expression of ICAM - 1 laid the foundation for skin inflammation therapeutics by using medicine latterly.%细胞间黏附分子-1(ICAM-1)是白细胞和角质细胞之间相互作用的必需因子,角质细胞中ICAM-1表达的上调与多种皮肤炎症相关.本研究为了优化γ-干扰素(IFN-γ)诱导HaCaT细胞ICAM-1表达的条件,用不同浓度的IFN-γ诱导HaCaT细胞不同时间,流式细胞仪检测ICAM-1表达.结果发现选用1 000U/mL的剂量诱导HaCaT细胞24h ICAM-1的表达是最高的.从而表明IFN-γ可以上调ICAM-γ的表达,为后期药物治疗皮肤炎症奠定基础.

  9. Vascular endothelial growth factor up-regulates the expression of intracellular adhesion molecule-1 in retinal endothelial cells via reactive oxygen species, but not nitric oxide

    Institute of Scientific and Technical Information of China (English)

    ZHANG Xiao-ling; WEN Liang; CHEN Yan-jiong; ZHU Yi

    2009-01-01

    Background The vascular endothelial growth factor (VEGF) is involved in the initiation of retinal vascular leakage and nonperfusion in diabetes. The intracellular adhesion molecule-1 (ICAM-1) is the key mediator of the effect of VEGFs on retinal leukostasis. Although the VEGF is expressed in an early-stage diabetic retina, whether it directly up-regulates ICAM-1 in retinal endothelial cells (ECs) is unknown. In this study, we provided a new mechanism to explain that VEGF does up-regulate the expression of ICAM-1 in retinal ECs.Methods Bovine retinal ECs (BRECs) were isolated and cultured. Immunohistochemical staining was performed to identify BRECs. The cultured cells were divided into corresponding groups. Then, VEGF (100 ng/ml) and other inhibitors were used to treat the cells. Cell lysate and the cultured supernatant were collected, and then, the protein level of ICAM-1 and phosphorylation of the endothelial nitric oxide synthase (eNOS) were detected using Western blotting. Griess reaction was used to detect nitric oxide (NO).Results Western blotting showed that the VEGF up-regulated the expression of ICAM-1 protein and increased phosphorylation of the eNOS in retinal ECs. Neither the block of NO nor protein kinase C (PKC) altered the expression of ICAM-1 or the phosphorylation of eNOS. The result of the Western blotting also showed that inhibition of phosphatidylinositol 3-kinase (PI3K) or reactive oxygen species (ROS) significantly reduced the expression of ICAM-1. Inhibition of PI3K also reduced phosphorylation of eNOS. Griess reaction showed that VEGF significantly increased during NO production. When eNOS was blocked by L-NAME or PI3K was blocked by LY294002, the basal level of NO production and the increment of NO caused by VEGF could be significantly decreased.Conclusion ROS-NO coupling in the retinal endothelium may be a new mechanism that could help to explain why VEGF induces ICAM-1 expression and the resulting leukostasis in diabetic retinopathy.

  10. Growth hormone increases vascular cell adhesion molecule 1 expression

    DEFF Research Database (Denmark)

    Hansen, Troels Krarup; Fisker, Sanne; Dall, Rolf;

    2004-01-01

    We investigated the impact of GH administration on endothelial adhesion molecules, vascular cell adhesion molecule-1 (VCAM-1) and E-selectin, in vivo and in vitro. Soluble VCAM-1, E-selectin, and C-reactive protein concentrations were measured before and after treatment in 25 healthy subjects...... and 25 adult GH-deficient (GHD) patients randomized to GH treatment or placebo. Furthermore, we studied the direct effect of GH and IGF-I and serum from GH-treated subjects on basal and TNF alpha-stimulated expression of VCAM-1 and E-selectin on cultured human umbilical vein endothelial cells. Baseline...... levels of VCAM-1, but not E-selectin, were significantly lower in GHD patients than in healthy subjects (362 +/- 15 microg/liter vs. 516 +/- 21 microg/liter, P treatment, compared with placebo [net difference between groups 151.8 microg/liter (95...

  11. The Serum Changes of Neuron-Specific Enolase and Intercellular Adhesion Molecule-1 in Patients With Diffuse Axonal Injury Following Progesterone Administration: A Randomized Clinical Trial

    Science.gov (United States)

    Shahrokhi, Nader; Soltani, Zahra; Khaksari, Mohammad; Karamouzian, Saeid; Mofid, Behshad; Asadikaram, Gholamreza

    2016-01-01

    Background Improvement of neurologic outcome in progesterone-administered patients with diffuse axonal injury (DAI) has been found in a recent study. Also, there has been interest in the importance of serum parameters as predictors of outcome in traumatic brain injury. Objectives The aim of this study was to examine the effect of progesterone administration on serum levels of neuron-specific enolase (NSE), and intercellular adhesion molecule-1 (ICAM-1) in clinical DAI. Patients and Methods In this study, the serum levels of ICAM-1 and NSE of 32 male DAI patients (18 - 60 years of age, a Glasgow coma scale of 12 or less, and admitted within 4 hours after injury) who were randomized for a controlled phase II trial of progesterone were analyzed. The analysis was performed between the control and progesterone groups at admission time, and 24 hours and six days after DAI, respectively. Results A reduction in the serum level of ICAM-1 was noticed in the progesterone group 24 hours after the injury (P < 0.05). There was no significant difference in the serum level of NSE between the study groups during evaluation. At 24 hours after the injury, the level of ICAM-1 in the control group was higher than that at admission time (P < 0.05). The lowest level of NSE in the two groups was seen six days after DAI (P < 0.01). Conclusions In summary, progesterone administration reduced serum ICAM-1, and whereby may attenuate blood brain barrier disruption, the latter needs further investigation for confirmation.

  12. High-density lipoprotein of patients with breast cancer complicated with type 2 diabetes mellitus promotes cancer cells adhesion to vascular endothelium via ICAM-1 and VCAM-1 upregulation.

    Science.gov (United States)

    Huang, Xiaoqin; He, Dan; Ming, Jia; He, Yubin; Zhou, Champion; Ren, Hui; He, Xin; Wang, Chenguang; Jin, Jingru; Ji, Liang; Willard, Belinda; Pan, Bing; Zheng, Lemin

    2016-02-01

    Adhesion of disseminating tumor cells to vascular endothelium is a pivotal starting point in the metastasis cascade. We have shown previously that diabetic high-density lipoprotein (HDL) has the capability of promoting breast cancer metastasis, and this report summarizes our more recent work studying the role of abnormal HDL in facilitating the adhesion of the circulating tumor cells to the endothelium. This is an initiating step in breast cancer metastasis, and this work assesses the role of ICAM-1 and VCAM-1 in this process. MDA-MB-231, MCF 7, and human umbilical vein endothelial cells (HUVECs) were treated with normal HDL from healthy controls (N-HDL), HDL from breast cancer patients (B-HDL), or HDL from breast cancer patients complicated with type 2 diabetes mellitus (BD-HDL), and the cell adhesion abilities were determined. ICAM-1 and VCAM-1 expression as well as the protein kinase C (PKC) activity were evaluated. The effect of PKC inhibitor and PKC siRNA on adhesion was also studied. The immunohistochemical staining of ICAM-1, VCAM-1, and E-selectin from breast cancer patients and breast cancer patients complicated with type 2 diabetes mellitus (T2DM) were examined. Our results indicate that BD-HDL promoted an increase in breast cancer cell adhesion to HUVECs and stimulated higher ICAM-1 and VCAM-1 expression on the cells surface of both breast cancer and HUVEC cells, along with the activation of PKC. Increased tumor cell (TC)-HUVEC adhesion, as well as ICAM-1 and VCAM-1 expression induced by BD-HDL, could be inhibited by staurosporine and PKC siRNA. In addition, a Db/db type 2 diabetes mouse model has more TC-Vascular Endothelium adhesion compared to a normal model. However, BD patients have a lower expression of ICAM-1, VCAM-1, and E-selectin in their tumor tissues. BD-HDL facilitates the adhesion of tumor cells to vascular endothelium by upregulating the expression of ICAM-1 and VCAM-1, thereby promoting the initial progression of breast cancer metastasis

  13. Effects of fosinopril and valsartan on expressions of ICAM-1 and NO in human umbilical vein endothelial cells

    Institute of Scientific and Technical Information of China (English)

    管思明; 王斌

    2003-01-01

    ObjectiveTo investigate the effects of fosinopril and valsartan on the expression of intercellular adhesion molecule-1 (ICAM-1) and nitric oxide (NO) induced by oxidizlls. MethodsThe levels of NO, ICAM-1, and nitric oxide synthase (NOS) were determined using the nitrate reductase method, ELISA, immunohistochemical and image analyses.ResultsThe ox-LDL can significantly increase the expression of ICAM-1 and inhibit theexpression of NO and NOS in a dose-dependent manner. Fosinopril and valsartancan significantly inhibit these roles of ox-LDL. The roles of fosinopril and valsartan were not significantly different. ConclusionFosinopril and valsartan inhibit oxidized LDL-induced expression of ICAM-1and increase the expression of NO in human umbilical vein endothelial cells, which is one of the mechanisms of antiatherosclerosis.

  14. A Novel Domain Cassette Identifies Plasmodium falciparum PfEMP1 Proteins Binding ICAM-1 and Is a Target of Cross-Reactive, Adhesion-Inhibitory Antibodies

    DEFF Research Database (Denmark)

    Bengtsson, Anja; Jørgensen, Louise; Rask, Thomas Salhøj;

    2013-01-01

    -exposed children. Our study challenges earlier conclusions that group A PfEMP1 proteins are not central to ICAM-1-specific IE adhesion and support the feasibility of developing a vaccine preventing cerebral malaria by inhibiting cerebral IE sequestration. The Journal of Immunology, 2013, 190: 240-249....

  15. Large-scale genomic studies reveal central role of ABO in sP-selectin and sICAM-1 levels

    NARCIS (Netherlands)

    M. Barbalic (maja); J. Dupuis (Josée); A. Dehghan (Abbas); J.C. Bis (Joshua); R.C. Hoogeveen (Ron); R. Schnabel (Renate); V. Nambi (Vijay); M. Bretler (Monique); N.L. Smith (Nicholas); A. Peters (Annette); C. Lu (Chao); R.P. Tracy (Russell); N. Aleksic (Nena); J. Heeriga (Jan); J.F. Keaney (John); K. Rice (Kenneth); G.Y. Lip (Gregory); R.S. Vasan (Ramachandran Srini); N.L. Glazer (Nicole); M.G. Larson (Martin); A.G. Uitterlinden (André); J.F. Yamamoto (Jennifer); P. Durda (Peter); T. Haritunians (Talin); B.M. Psaty (Bruce); E.A. Boerwinkle (Eric); A. Hofman (Albert); W. Koenig (Wolfgang); N.S. Jenny (Nancy); J.C.M. Witteman (Jacqueline); C. Ballantyne (Christie); E.J. Benjamin (Emelia)

    2010-01-01

    textabstractP-selectin and intercellular adhesion molecule-1 (ICAM-1) participate in inflammatory processes by promoting adhesion of leukocytes to vascular wall endothelium. Their soluble levels have been associated with adverse cardiovascular events. To identify loci affecting soluble levels of P-s

  16. A study on the pathogenesis of the radiation pneumonitis. Alterations in pulmonary mRNA encoding adhesion molecules ICAM-1, VCAM-1, and P-selectin following thoracic irradiation in mice

    Energy Technology Data Exchange (ETDEWEB)

    Tsujino, Kayoko; Kodama, Akihisa; Kono, Michio [Kobe Univ. (Japan). School of Medicine

    1997-12-01

    To investigate the role of the adhesion molecules in the pathogenesis of the radiation pneumonitis, we quantified the mRNA expression of the adhesion molecules in the lung by Northern blot method following whole thorax irradiation to C57BL/6J mice. After irradiation of 12 Gy to the whole thorax, there were increase of mRNA for ICAM-1 by 42% at 4 hours (p<0.05), 76% at 24 hours (p<0.01) and 51% at 48 hours (p<0.05) compared with controls. And it returned to control level at 1 week. No significant change was observed thereafter until 8 weeks. The expression of VCAM-1 mRNA were also increased by 49% (p<0.01) at 12 hours and were still increased by 25% at 1 week. P-selectin mRNA as transiently increased by 59% at 12 hours. We examined the relationship between the ICAM-1 induction and the radiation dose, and found that ICAM-1 expression was increased by 3 Gy of irradiation and it was increased in radiation dose dependent manner up to 24 Gy. These early inductions of mRNA for ICAM-1, VCAM-1 and P-selectin in mice lungs following thoracic irradiation were transient but significant, and they were one of the most immediate change reported in vivo. It is suggested that these adhesion molecules are possibly related to the pathogenesis of the radiation pneumonitis. (author)

  17. Adhesion of human basophils, eosinophils, and neutrophils to interleukin 1-activated human vascular endothelial cells: contributions of endothelial cell adhesion molecules

    OpenAIRE

    1991-01-01

    Cytokines such as interleukin 1 (IL-1) promote adhesiveness in human umbilical vein endothelial cells for leukocytes including basophils, eosinophils, and neutrophils, and induce expression of adherence molecules including ICAM-1 (intercellular adhesion molecule-1), ELAM-1 (endothelial-leukocyte adhesion molecule-1), and VCAM-1 (vascular cell adhesion molecule-1). In the present study, blocking monoclonal antibodies (mAb) recognizing ICAM-1, ELAM-1, and VCAM-1 have been used to compare their ...

  18. Cocaine-associated retiform purpura: a C5b-9-mediated microangiopathy syndrome associated with enhanced apoptosis and high levels of intercellular adhesion molecule-1 expression.

    Science.gov (United States)

    Magro, Cynthia M; Wang, Xuan

    2013-10-01

    Cocaine-associated retiform purpura is a recently described entity characterized by striking hemorrhagic necrosis involving areas of skin associated with administration of cocaine. Levamisole, an adulterant in cocaine, has been suggested as the main culprit pathogenetically. Four cases of cocaine-associated retiform purpura were encountered in the dermatopathology practice of C. M. Magro. The light microscopic findings were correlated with immunohistochemical and immunofluorescence studies. All 4 cases showed a very striking thrombotic diathesis associated with intravascular macrophage accumulation. Necrotizing vasculitis was noted in 1 case. Striking intercellular adhesion molecule-1 (ICAM-1)/CD54 expression in vessel wall along with endothelial expression of caspase 3 and extensive vascular C5b-9 deposition was observed in all biopsies examined. Cocaine-induced retiform purpura is a C5b-9-mediated microvascular injury associated with enhanced apoptosis and prominent vascular expression of ICAM-1, all of which have been shown in prior in vitro and in vivo murine models to be a direct effect of cocaine metabolic products. Antineutrophilic cytoplasmic antibody and antiphospholipid antibodies are likely the direct sequelae of the proapoptotic microenvironment. The inflammatory vasculitic lesion could reflect the downstream end point reflective of enhanced ICAM-1 expression and the development of antineutrophilic cytoplasmic antibody. Levamisole likely works synergistically with cocaine in the propagation of this syndromic complex. PMID:23392134

  19. Lipopolysaccharide Binding Protein, Soluble-Intercellular Adhesion Molecule-1, Procalcitonin, and Protein C Activity and Clinical Outcome in Systemic Inflammatory Response Syndrome (SIRS or Sepsis Patients

    Directory of Open Access Journals (Sweden)

    Dewi Muliaty

    2009-04-01

    Full Text Available BACKGROUND: Biochemical markers may be used in diagnosis, prognostic and monitoring treatment and therapy for sepsis patients. In this study we used Lipopolysacharide Binding Protein (LBP, serum-Intercellular Adhesion Molecule-1 (ICAM-1, Procalcitonin (PCT and protein C activity. LBP is related to lipopolysachharide or gram-negative bacterial endotoxin which bound to LBP and induced inflammatory response. ICAM-1 is associated with endothelial dysfunction in response to systemic inflammatory and septic condition. PCT increased in bacterial infection and in severe systemic inflammatory. Role of Protein C is protecting the intravascular system to systemic inflammation, sepsis and the concomitant intravascular coagulopathy. The aim of this study was to examine the associations between levels of serum LBP, sICAM-1, PCT, and protein C activity with the clinical outcome of SIRS or sepsis patients. METHODS: We included 19 post surgery patients with SIRS criteria from intensive care unit (ICU and evaluated the level of LBP serum with Chemiliuminescent Enzyme Immunoassay (Diagnostic Product Co., ICAM-1 with ELISA (R&D System, PCT with immunochromatography (BRAHMS, protein C activity with chromogenic method (Dade Behring. We performed the samples serially at the first admission of patients and after 72 hours. Data were analysed by non-parametric with Wilcoxon test and Mann-Whitney test. Correlation study between biomarkers calculated by Kendall’s tau and Spearman’s rho. RESULTS: Of 19 patients, 9 (47,4% died and 10 (52,6% surviving. The level of LBP serum decreased after 72 hours in surviving-sepsis patients, and increased in nonsurviving sepsis patients with significant different levels at 72 hours examination (p0.05. In all patients were found high level of PCT serum since the first admission examination, decreasing levels were occurred significantly in surviving patients after 72 hours (p0.05 both in surviving and non-surviving patients. CONCLUSIONS

  20. Expression of ICAM-1 in mice with radiation induced lung injury

    International Nuclear Information System (INIS)

    Objective: To observe the expression of intercellular adhesion molecule-1 (ICAM-1) in mice with radiation induced lung injury and to study the function of ICAM-1. Methods: The thoraces of C57BL/6 mice were exposed to either sham irradiation or single fraction of 12 Gy. Two groups were defined as received sham-irradiation (C group) and underwent irradiation (X group). Mice were sacrificed at hours 1, 24, 72 and weeks 1, 2, 4, 8, 16, 24 after irradiation. The lung tissues were removed and processed for definitive analysis, including HE and Masson staining, the hydroxyproline content, the immunohistochemistry and the real-time quantitative RT-PCR. Results: Compared with C group, there was a significant histological and pathologic change in X group. And there was a significantly elevated level of positive cell counts of ICAM-1 and inflammatory cells in X group (P<0.01). Similarly, there was a significantly elevated level of hydroxyproline in X group(P<0.05). Moreover, the results of real-time quantitative RT-PCR showed that the relative mRNA expression of cytokine ICAM-1 in X group was significantly higher than that of C group(P<0.01). Conclusions: As an important cytokine in radiation-induced lung injury, ICAM-1 can not only mediate the inflammation cells adherence and infiltration, but also be involved in radiation induced lung fibrosis. (authors)

  1. Expression of intercellular adhesion molecule-1 and clinical significance in gastric carcinoma%胃癌中细胞间黏附分子1的表达及其临床意义

    Institute of Scientific and Technical Information of China (English)

    牟时斌; 高峰

    2015-01-01

    Objective To observe the expression of intercellular adhesion molecule-1 (ICAM-1 )in gastric carcinoma and its adjacent tissues and two cultured gastric carcinoma cell lines,so as to explore its value in the clinical practice.Methods The expression of ICAM-1 in 90 cases of gastric carcinoma tissues,40 cases of adjacent tissues and two cultured gastric carcinoma cell lines (MKN45 and SGC-7901 ) was determined by Western blot and immunohistochemistry(IHC).The gastric carcinoma tissues were then divided into ICAM-1-positive group (n =68) and ICAM-1-negative group (n =22).Results The expression of ICAM-1 in gastric carcinoma tissues (4.5±0.3)and gastric carcinoma cell lines (5.6 ± 0.2 )were significantly higher than that in the adjacent tissues (1.0 ± 0.1,P <0.01).The positive rate of ICAM-1 in gastric carcinoma tissues was 75.6%(68/90),remarkably higher than that in the adjacent tissues 32.5%(13/40)(P <0.01).Compared with those in the ICAM-1-negative group,ICAM-1-positive group had larger tumor size,more serious infiltration and more common nerve invasion (P <0.01).Furthermore,the recurrence rate in the ICAM-1-positive group was markedly higher than that in the ICAM-1-negative group (67.6% vs 22.7%,P <0.05)and the five year survival rate in the ICAM-1-positive group was prominently lower than that in the ICAM-1-negative group (61.1% vs 80.0%,P <0.05).Conclusion The overexpression of ICAM-1 in gastric cancer tissues predicted more intensive invasion and poorer prognosis.%目的:研究细胞间黏附分子1(ICAM-1)在胃癌组织、癌旁胃组织及胃癌细胞系中的表达及对临床实践的价值。方法从90例胃癌组织、40例癌旁胃组织及2种胃癌细胞系(MKN45、SGC-7901)中提取蛋白质,以蛋白质印迹法检测 ICAM-1的表达水平;对90例胃癌组织以 ICAM-1为一抗进行免疫组织化学(IHC)检测,并根据 IHC 结果把患者分为 ICAM-1阳性组(68例)和 ICAM-1阴性组(22例)。结果胃癌组织及胃癌细胞系中 ICAM

  2. Characterization of the oligodeoxynucleotide-mediated inhibition of interferon-gamma-induced major histocompatibility complex class I and intercellular adhesion molecule-1.

    Science.gov (United States)

    Ramanathan, M; Lantz, M; MacGregor, R D; Garovoy, M R; Hunt, C A

    1994-10-01

    The major histocompatibility complex (MHC) Class I and II genes and intercellular adhesion molecule-1 (ICAM-1) are regulated by interferon-gamma in a variety of cell types. We have previously shown that the oligodeoxynucleotide 5'-GGG GTT GGT TGT GTT GGG TGT TGT GT-RNH2 (oligo I) inhibits the interferon-gamma-mediated enhancement of MHC Class I and ICAM-1 proteins in the K562 cell line. We have now investigated the mechanism of action of oligo I and report that it acts by inhibiting the binding of interferon-gamma to cells. We also show that the dose-response curves, the selectivity profile, and the kinetics of oligo I are consistent with this novel mechanism of action. The dose-response curves for oligo I, obtained using antibodies against the MHC Class I heavy chain, beta 2-microglobulin, or ICAM-1, are almost superimposable at each observation time. MHC Class I induction by 6400 units/ml interferon-alpha or interferon-beta or ICAM-1 enhancement by 800 units/ml tumor necrosis factor-alpha is not inhibited by oligo I. However, the synergistic induction of MHC Class I by mixtures of tumor necrosis factor-alpha and interferon-gamma is inhibited. Oligo I belongs to a class of active oligodeoxynucleotides that inhibits interferon-gamma-induced MHC Class I and ICAM-1 in K562 cells. The activity and potency is sequence-dependent, but remarkably different sequences can have comparable effects. The activity of oligo I in the HeLa S3 cell line inhibits the interferon-gamma-mediated enhancement of both ICAM-1 and MHC Class II DR and the interferon-gamma-mediated reduction in transferrin receptor expression. Thus, oligo I appears to specifically inhibit interferon-gamma-induced changes in protein expression, which is consistent with oligo I acting at an early step(s) in the induction process. Taken together, our results show that oligo I exerts its effects by inhibiting the association of interferon-gamma with the cell surface, which is a novel mechanism of action for

  3. Cerebrospinal fluid and plasma concentration of soluble intercellular adhesion molecule1, vascular cell adhesion molecule1 and endothelial leukocyte adhesion molecule in patients with acute ischemic b

    Directory of Open Access Journals (Sweden)

    Selaković Vesna M.

    2003-01-01

    Full Text Available Background. Leukocyte migration into the ischemic area is a complex process controlled by adhesion molecules (AM in leukocytes and endothelium, by migratory capacity of leukocytes and the presence of hemotaxic agents in the tissue. In this research it was supposed that in the blood and cerebrospinal fluid (CSF of patients in the acute phase of ischemic brain disease (IBD there were relevant changes in the concentration of soluble AM (sICAM-1 sVCAM-1 and sE-selectin, that could have been the indicators of the intensity of damaging processes in central nervous system (CNS. Methods. The study included 45 IBD patients, 15 with transient ischemic attack (TIA 15 with reversible ischemic attack (RIA, and 15 with brain infarction (BI of both sexes, mean age 66±7. Control group consisted of 15 patients with radicular lesions of discal origin, subjected to diagnostic radiculography without the signs of interruption in the passage of CSF. Changes of selected biochemical parameters were determined in all patients in frame 72 hours since the occurence of an ischemic episode. Concentrations of soluble AM were determined in plasma and CSF by ELISA. Total number of leukocytes (TNL in peripheral blood was determined by hematological analyzer. Results. The results showed that during the first 72 hrs of IBD significant increases occured in TNL and that the increase was progressive compared to the severeness of the disease. Significant increase of soluble AM concentration was shown in plasma of IBD patients. The increase was highest in BI somewhat lower in RIA and the lowest in TIA patients compared to the control. In CSF concentrations of sICAM-1, sVCAM-1 and sE-selectin demonstrated similar increasing trend as in plasma. Conclusion. TNL, as well as the soluble AM concentrations in plasma and CSF, were increased during the acute IBD phase and progressive in relation to the severeness of the disease, so that they might have been the indicators of CNS inflammatory

  4. Expression of inflammation related factors iNOS and ICAM-1 in endothelial cells induced by C-reactive protein

    OpenAIRE

    Song, Xu-Dong; Chen, Ai-Hua; He, Fei; Li, Zhi-Liang; Ying-feng LIU

    2011-01-01

    Objective To investigate the expression of inducible nitric oxide synthase(iNOS) and intercellular cell adhesion molecule-1(ICAM-1) in endothelial cells induced by C-reactive protein(CRP) and its corresponding mechanisms.Methods Human umbilical cord vein endothelial cells(HUVEC) were treated with different concentrations of CRP or with phosphate buffered solution as control,and RT-PCR was used for measurement of the expression of ICAM-1 mRNA induced by CRP in HUVECs.HUVEC were treated with CR...

  5. Association of ICAM-1 K469E polymorphism with dengue infection in North Indian population.

    Science.gov (United States)

    Sharma, Swati; Singh, Satyendra K; Kakkar, Kavita; Nyari, Nikky; Singh, Dharamveer; Dhole, Tapan N; Kashyap, Rajesh; Hasan, Saba

    2016-07-01

    Dengue infection is caused by flavivirus is one of the leading cause of mortality. There are certain factors which play role in the transformation of a mild form of the disease (DF) into a severe form (DHF) but the most important ones are: viral strain virulence, host genetics, and host immune status. In severe dengue infection, plasma leakage occurs due to vascular endothelial cell activation through expression of adhesion molecule like intercellular cell adhesion molecule-1 (ICAM-1). A total of 100 dengue patients (DF; n = 53 and DHF/DSS; n = 47) and 200 healthy controls were included in the study. ICAM-1 K469E genotyping was done by polymerase chain reaction-restriction fragment length polymorphism (PCR- RFLP). Expression of ICAM-1 mRNA was done by Real time reverse transcription- PCR (rRT-PCR). Patients with homozygous genotype (EE) have 3.22 fold risk (P = 0.008) of developing severe form of disease (DHF/DSS) as compared to other genotypes. Patients with DHF/DSS exhibit higher expression of ICAM-1 mRNA as compared to dengue fever and controls (P = 0.001 and < 0.001). Patients (DHF/DSS) with homozygous (EE) genotype exhibit higher expression of ICAM-1 mRNA when compared with wild type (KK) genotype (P = 0.005). This study suggests a possible association between the ICAM-1 polymorphism and the disease severity. PMID:27179462

  6. EFFECT OF PREOPERATIVE GLUTAMINE ADMINISTRATION ON ICAM-1 EXPRESSION IN RAT LUNG INDUCED BY INTESTINAL ISCHEMIA-REPERFUSION

    Institute of Scientific and Technical Information of China (English)

    GENG Gui-qi; JIANG Hong; ZHU Ye-sen

    2008-01-01

    Objective To evaluate the effect of preoperative glutamine administration on intracellular adhesion molecule-1 (ICAM-1) expression in rat lung induced by intestinal ischemia-reperfusion( I/R ). Methods Sprague-Dawley rats (n = 25) were randomly divided into 5 groups: sham group ( sham surgery), glutamine groups (three different doses) and control group. All groups except sham were subjected to intestinal I/R injury, and superior mesenteric artery (SMA) occluded for 60 min followed by 90 min of reperfusion. Lung injury was evaluated with Evans blue dye concentration and histopathologic examination. The immunohistochemical expression and mRNA expression of ICAM-1 were measured with immunohistochemical staining and RT-PCR method respectively. The level of myeloperoxidase (MPO) was also measured with biochemistry method. Results Intestinal I/R resulted in lung injury characterized by an increase in Evans blue dye concentration, neutrophil sequestration, and obvious staining for expression of pulmonary ICAM-1, compared with sham group. The expression of ICAM-1 and the level of MPO in rat lung were lower in glutamine groups compared with control group. Conclusion I-R injury increases the expression of ICAM-1 within the lung. This may contribute to the migration, accumulation and activation of polymorphanuclear neutrophils (PMNs) after such injury. Preoperative glutamine administration attenuates rat lung injury induced by intestinal I-R, and inhibiting ICAM-1 expression maybe one of the potential mechanisms.

  7. Modulation of human leukocyte antigen and intracellular adhesion molecule-1 surface expression in malignant and nonmalignant human thyroid cells by cytokines in the context of extracellular matrix.

    Science.gov (United States)

    Miller, A; Kraiem, Z; Sobel, E; Lider, O; Lahat, N

    2000-11-01

    Interactions between malignant cells and their environment are achieved via cell-surface receptors and adhesion molecules. The extracellular matrix (ECM) and ECM-bound cytokines modulate the expression of cell-surface molecules on target malignant cells, which may lead to changes in their susceptibility to cytolysis, in their ability to present antigens, and in the induction of local immune-cell activation and patrol. Eventually, these alterations may culminate in either the destruction, or escape and proliferation, of the tumor. We studied the effects of the ECM and its components in a "naive" form or following binding of the inflammatory cytokines interferon gamma (IFNgamma) and tumor necrosis factor alpha (TNFalpha) on the surface expression of human leukocyte antigen (HLA) class-I, HLA class-II (HLA-DR), and intracellular adhesion molecule-1 (ICAM-1), on nonmalignant and malignant thyroid cells. The basal expression of HLA class-I molecules was not significantly changed either by naive ECM and its components or by ECM-bound cytokines. ECM synergized with IFNgamma and TNFalpha in inducing HLA-DR molecules on nonmalignant and malignant thyrocytes, with higher HLA-DR levels on the malignant cells. The laminin component, in particular, synergized with IFNgamma. Basal ICAM-1 expression on nonneoplastic cells was not significantly affected by the cytokines when grown in the absence of ECM, but was significantly upregulated when cells were cultured on ECM. In contrast, in malignant thyrocyte cultures, ECM significantly attenuated IFNgamma- and TNFalpha-mediated enhancement of ICAM-1 expression. We concluded that signals derived from ECM-embedded cytokines participate in the regulation of key thyroid cell surface molecules and, thus, may affect the final outcome of human thyroid malignancies. PMID:11128721

  8. Non-cysteine linked MUC1 cytoplasmic dimers are required for Src recruitment and ICAM-1 binding induced cell invasion

    Directory of Open Access Journals (Sweden)

    Gunasekara Nirosha

    2011-07-01

    Full Text Available Abstract Background The mucin MUC1, a type I transmembrane glycoprotein, is overexpressed in breast cancer and has been correlated with increased metastasis. We were the first to report binding between MUC1 and Intercellular adhesion molecule-1 (ICAM-1, which is expressed on stromal and endothelial cells throughout the migratory tract of a metastasizing breast cancer cell. Subsequently, we found that MUC1/ICAM-1 binding results in pro-migratory calcium oscillations, cytoskeletal reorganization, and simulated transendothelial migration. These events were found to involve Src kinase, a non-receptor tyrosine kinase also implicated in breast cancer initiation and progression. Here, we further investigated the mechanism of MUC1/ICAM-1 signalling, focusing on the role of MUC1 dimerization in Src recruitment and pro-metastatic signalling. Methods To assay MUC1 dimerization, we used a chemical crosslinker which allowed for the detection of dimers on SDS-PAGE. We then generated MUC1 constructs containing an engineered domain which allowed for manipulation of dimerization status through the addition of ligands to the engineered domain. Following manipulation of dimerization, we immunoprecipitated MUC1 to investigate recruitment of Src, or assayed for our previously observed ICAM-1 binding induced events. To investigate the nature of MUC1 dimers, we used both non-reducing SDS-PAGE and generated a mutant construct lacking cysteine residues. Results We first demonstrate that the previously observed MUC1/ICAM-1signalling events are dependent on the activity of Src kinase. We then report that MUC1 forms constitutive cytoplasmic domain dimers which are necessary for Src recruitment, ICAM-1 induced calcium oscillations and simulated transendothelial migration. The dimers are not covalently linked constitutively or following ICAM-1 binding. In contrast to previously published reports, we found that membrane proximal cysteine residues were not involved in

  9. Expression of pulmonary mRNA encoding ICAM-1, VCAM-1, and P-selectin following thoracic irradiation in mice

    Energy Technology Data Exchange (ETDEWEB)

    Tsujino, Kayoko; Kodama, Akihisa; Nanaoka, Noriyoshi; Maruta, Tsutomu; Kono, Michio [Kobe Univ. (Japan). School of Medicine

    1999-08-01

    Recent studies have revealed that ionizing radiation induces the expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and P-selectin in vitro. The purpose of this study was to investigate the expression of these adhesion molecules in mouse lung following whole thoracic irradiation. C57BL/6J mice were irradiated with a single dose of 12 Gy to the thoraces and sacrificed at 4, 12, 24, and 48 hours and 1, 2, 4, and 8 weeks after irradiation. Expression of total lung mRNA for ICAM-1, VCAM-1, and P-selectin was quantified by the Northern blot method and normalized to {beta}-actin. There were increases in mRNA for ICAM-1 of 42% at 4 hours (p<0.05), 76% at 24 hours (p<0.01), and 51% at 48 hours (p<0.05) compared with the controls. There returned to the control level at 1 week. The expression of VCAM-1 mRNA was also increased by 49% (p<0.01) at 12 hours and was still increased by 25% at 1 week. P-selectin mRNA was transiently increased by 59% at 12 hours. These early inductions of mRNA for ICAM-1, VCAM-1, and P-selectin in mouse lung following thoracic irradiation were transient but significant, and are one of the most immediate changes reported in vivo. (author)

  10. Pathogenic Actions of Cell Adhesion Molecule 1 in Pulmonary Emphysema and Atopic Dermatitis

    OpenAIRE

    Yoneshige, Azusa; Hagiyama, Man; Fujita, Mitsugu; Ito, Akihiko

    2015-01-01

    Cell adhesion mediated by adhesion molecules is of central importance in the maintenance of tissue homeostasis. Therefore, altered expression of adhesion molecules leads to the development of various tissue disorders involving cell activation, degeneration, and apoptosis. Nevertheless, it still remains unclear what initiates the altered expression of adhesion molecules and how the subsequent pathological cascades proceed. In this regard, cell adhesion molecule 1 (CADM1) is one of the candidat...

  11. Kinetics of human T-cell expression of LFA-1, IL-2 receptor, and ICAM-1 following antigenic stimulation in vitro

    DEFF Research Database (Denmark)

    Hviid, L; Felsing, A; Theander, T G

    1993-01-01

    in vitro is paralleled by differential kinetics in the expression of the T-cell adhesion and activation antigens leukocyte function-associated antigen 1 (LFA-1; CD11a/CD18), interleukin-2 receptor (IL-2R; CD25), and intercellular adhesion molecule 1 (ICAM-1; CD54). Furthermore, the changes in expression...... prestimulation levels, and CD25 expression was decreasing. This indicates that T-cell expression of all the 3 surface antigens examined is reversible. While this is in agreement with previous reports of the expression kinetics of IL-2R and ICAM-1, this is the first report indicating that the regulation of T...

  12. Regional gene expression of LOX-1, VCAM-1, and ICAM-1 in aorta of HIV-1 transgenic rats.

    Directory of Open Access Journals (Sweden)

    Anne Mette Fisker Hag

    Full Text Available BACKGROUND: Increased prevalence of atherosclerotic cardiovascular disease in HIV-infected patients has been observed. The cause of this accelerated atherosclerosis is a matter of controversy. As clinical studies are complicated by a multiplicity of risk-factors and a low incidence of hard endpoints, studies in animal models could be attractive alternatives. METHODOLOGY/PRINCIPAL FINDINGS: We evaluated gene expression of lectin-like oxidized-low-density-lipoprotein receptor-1 (LOX-1, vascular cell adhesion molecule-1 (VCAM-1, and intercellular adhesion molecule-1 (ICAM-1 in HIV-1 transgenic (HIV-1Tg rats; these genes are all thought to play important roles in early atherogenesis. Furthermore, the plasma level of sICAM-1 was measured. We found that gene expressions of LOX-1 and VCAM-1 were higher in the aortic arch of HIV-1Tg rats compared to controls. Also, the level of sICAM-1 was elevated in the HIV-1Tg rats compared to controls, but the ICAM-1 gene expression profile did not show any differences between the groups. CONCLUSIONS/SIGNIFICANCE: HIV-1Tg rats have gene expression patterns indicating endothelial dysfunction and accelerated atherosclerosis in aorta, suggesting that HIV-infection per se may cause atherosclerosis. This transgenic rat model may be a very promising model for further studies of the pathophysiology behind HIV-associated cardiovascular disease.

  13. Research on Inhibitory Effect of Momordica charantia L. Polyphenol on Vascular Endothelial Intercellular Adhesion Molecular-1 (ICAM-1) mRNA Abnormal Expression

    OpenAIRE

    Xuezheng Huang; Miaochao Chen; Peilong Xu

    2013-01-01

    The study held a research on the anti-oxidative damage effect and mechanism of Momordica charantia L. Polyphenol from gene level. Method: it tested the influence of Momordica charantia L. Polyphenol to human umbilical veins blood vessel endothelial cell strain (CRL-1730) ICAM-1 mRNA cellular expression caused by oxidative damage with RT-PCR method. Result: the experimental result indicated that the luminance and area values of electrophoretic band of 4, 5, and 6 with different doses of Momord...

  14. Aldosterone stimulates nuclear factor-kappa B activity and transcription of intercellular adhesion molecule-1 and connective tissue growth factor in rat mesangial cells via serum- and glucocorticoid-inducible protein kinase-1.

    Science.gov (United States)

    Terada, Yoshio; Ueda, Satoko; Hamada, Kazu; Shimamura, Yoshiko; Ogata, Koji; Inoue, Kosuke; Taniguchi, Yoshinori; Kagawa, Toru; Horino, Taro; Takao, Toshihiro

    2012-02-01

    Several clinical and experimental data support the hypothesis that aldosterone contributes to the progression of renal injury. To determine the signaling pathway of aldosterone in relation to fibrosis and inflammation in mesangial cells, we investigated the effects of aldosterone on expression and activation of serum- and glucocorticoid-inducible protein kinase-1 (SGK1), the activation of nuclear factor-kappa B (NF-κB activation, and the expressions of intercellular adhesion molecule-1 (ICAM-1) and connective tissue growth factor (CTGF). Aldosterone stimulated SGK1 expression, phosphorylation (Ser-256), and kinase activity. The increments of phosphorylation and expression of SGK1 induced by aldosterone were inhibited by mineralocorticoid receptor (MR) inhibitor (eplerenone). Aldosterone stimulated NF-κB activity measured by NF-κB responsive elements, luciferase assay, and the levels of inhibitor of kappa B (IκB) phosphorylation. This aldosterone-induced activation of NF-κB was inhibited by the transfection of dominant-negative SGK1. Furthermore, aldosterone augmented the promoter activities and protein expressions of ICAM-1 and CTGF. The effects of aldosterone on ICAM-1 and CTGF promoter activities and protein expressions were inhibited by the transfection of dominant-negative SGK1 and dominant-negative IκBα. We also found that the MR antagonist significantly ameliorated the glomerular injury and enhancements in SGK1, ICAM-1, and CTGF expressions induced by 1% sodium chloride and aldosterone in vivo. In conclusion, our findings suggest that aldosterone stimulates ICAM-1 and CTGF transcription via activation of SGK1 and NF-κB, which may be involved in the progression of aldosterone-induced mesangial fibrosis and inflammation. MR antagonists may serve as useful therapeutic targets for the treatment of glomerular inflammatory disease.

  15. ICAM-1-based rabies virus vaccine shows increased infection and activation of primary murine B cells in vitro and enhanced antibody titers in-vivo.

    Directory of Open Access Journals (Sweden)

    James E Norton

    Full Text Available We have previously shown that live-attenuated rabies virus (RABV-based vaccines infect and directly activate murine and human primary B cells in-vitro, which we propose can be exploited to help develop a single-dose RABV-based vaccine. Here we report on a novel approach to utilize the binding of Intracellular Adhesion Molecule-1 (ICAM-1 to its binding partner, Lymphocyte Function-associated Antigen-1 (LFA-1, on B cells to enhance B cell activation and RABV-specific antibody responses. We used a reverse genetics approach to clone, recover, and characterize a live-attenuated recombinant RABV-based vaccine expressing the murine Icam1 gene (rRABV-mICAM-1. We show that the murine ICAM-1 gene product is incorporated into virus particles, potentially exposing ICAM-1 to extracellular binding partners. While rRABV-mICAM-1 showed 10-100-fold decrease in viral titers on baby hamster kidney cells compared to the parental virus (rRABV, rRABV-mICAM-1 infected and activated primary murine B cells in-vitro more efficiently than rRABV, as indicated by significant upregulation of CD69, CD40, and MHCII on the surface of infected B cells. ICAM-1 expression on the virus surface was responsible for enhanced B cell infection since pre-treating rRABV-mICAM-1 with a neutralizing anti-ICAM-1 antibody reduced B cell infection to levels observed with rRABV alone. Furthermore, 100-fold less rRABV-mICAM-1 was needed to induce antibody titers in immunized mice equivalent to antibody titers observed in rRABV-immunized mice. Of note, only 10(3 focus forming units (ffu/mouse of rRABV-mICAM-1 was needed to induce significant anti-RABV antibody titers as early as five days post-immunization. As both speed and potency of antibody responses are important in controlling human RABV infection in a post-exposure setting, these data show that expression of Icam1 from the RABV genome, which is then incorporated into the virus particle, is a promising strategy for the development of a

  16. The Relationship between Eating Disorders and ICAM-1, E-selection and Ghrelin Resting Level in Overweight People

    Directory of Open Access Journals (Sweden)

    Gholamreza Sharifi

    2014-11-01

    Full Text Available Introduction There is an agreement that eating disorder is related to psychological characteristics and on the other hand, level of ghrelin hormone, Intercellular adhesion molecule-1 (ICAM-1 and E-selection also change during eating disorders. We aimed to study the relationship between eating disorders and rest levels, ICAM-1, E-selection, and ghrelin hormone in obese people. Materials and Methods  In this quasi-experimental study, 120 obese men (25-30 years old were purposefully selected. Then the data about their eating disorders gathered with eating attitudes test (EAT-26 questionnaire. In the next phase in the rest condition and after overnight fasting, blood samples are collected for measurement of rest levels, ICAM-1, E-selection, and ghrelin hormone. Finally the data were analyzed with appropriate statistical tests in SPSS version 18. Results Mean and deviation of rest levels, ICAM-1, E-selection, and ghrelin hormone were respectively 3064.19, 61.5±19.7, and 2.5±1.5 and there was not any statistical significance relationship between eating disorders ICAM-1, E-selection, and ghrelin hormone in obese men (P

  17. Inhibitory Effects of Atorvastatin on the mRNA Expression of ICAM-1 and VCAM-1 Activated by TNF-α in Cultured Human Umbilical Vein Endothelial Cells

    Institute of Scientific and Technical Information of China (English)

    Zhiming Yang; Zhanhai Li; Gaiying Fan; Bin Liang; Ying Ma; Chuanshi Xiao; Yuming Kang

    2007-01-01

    To investigate the effects of atorvastatin on the mRNA expression of intercellular adhesion molecule-1 ( ICAM-1 ) and vascular cell adhesion molecule-1 ( VCAM-1 ) activated by TNF-α in cultured human umbilical vein endothelial cells (HUVEC).Methods and Results Lactic dehydrogenase (LDH) activity in the culture media increased when HUVEC were incubated with TNF-α,suggesting a cytotoxic effect of TNF-α on HUVEC.The mRNA expression of ICAM-1 and VCAM-1 increased in HUVEC incubated with 10μg/L TNF-α and reached peak in HUVEC incubated with 30μg/L TNF-α.The mRNA expression of ICAM-1 and VCAM-1 in HUVEC incubated with 30μg/L TNF-α began to increase at 6 h,reached peak at 48 h,and kept a plateau until 72 h.Atorvastatin dose-dependently inhibited the mRNA expressions of ICAM-1 and VCAM-1 activated by incubating HUVEC with 30μg/L TNF-α for 48 hours.Conclusions Atorvastatin might stabilize plaque and decelerate the process of AS by inhibiting the mRNA expressions of ICAM-1 and VCAM-1.

  18. Expression of inflammation related factors iNOS and ICAM-1 in endothelial cells induced by C-reactive protein

    Directory of Open Access Journals (Sweden)

    Xu-dong SONG

    2011-08-01

    Full Text Available Objective To investigate the expression of inducible nitric oxide synthase(iNOS and intercellular cell adhesion molecule-1(ICAM-1 in endothelial cells induced by C-reactive protein(CRP and its corresponding mechanisms.Methods Human umbilical cord vein endothelial cells(HUVEC were treated with different concentrations of CRP or with phosphate buffered solution as control,and RT-PCR was used for measurement of the expression of ICAM-1 mRNA induced by CRP in HUVECs.HUVEC were treated with CRP of 1mg/L,5mg/L,20mg/L,or with phosphate buffered solution,and expressions of ICAM-1 and iNOS protein in HUVECs were detected by cellular enzyme linked immunosorbent assay(ELISA.Results In groups of 1mg/L,5mg/L and 10mg/L CRP,no different effects on expression of ICAM-1 mRNA in HUVECs was found when compared with control group,whereas the expression of ICAM-1 mRNA was elevated in the group of 20mg/L CRP by 1.48 folds compared with that in control group.Similarly,in groups of 1mg/L and 5mg/L CRP there was no significant difference in the expressions of ICAM-1 and iNOS in HUVECs compared with that in control group(P > 0.05,whereas the expressions of ICAM-1 and iNOS protein were increased significantly in group of 20mg/L CRP compared with that in other groups(P< 0.01.Conclusions Although CRP may induce the expression of inflammatory factors in endothelial cells,the present experioment showed that CRP had no significant effects on inflammatory factors in endothelial cells at normal physiological level,and it gave inducible effects at higher concentration(20mg/L only.

  19. The effect of antibodies against cell-surface adhesion molecules (LFA-1{alpha} and ICAM-1) on the migration and localization of {sup 99m}Tc-labeled leukocytes in acute infection

    Energy Technology Data Exchange (ETDEWEB)

    Amartey, J.K.; Parhar, R.S.; Al-Sedairy, S.T

    1997-08-01

    The deficiency of adhesion molecules on leukocytes could severely impair their ability to migrate and perform effective immunological functions leading to clinical situations such as LAD (leukocyte adhesion deficiency) syndrome. We investigated the effects of blocking anti-LFA-1{alpha} and ICAM-1 antibody-treated {sup 99m}Tc-labeled leukocytes on the migration and localization to the site of E. coli-induced acute infection in CBA/J mice. A significant inhibition of migration and localization of antibody-treated leukocytes to the site of infection was observed, reaffirming the vital role of these adhesion molecules, especially during scintigraphic examination of patients for deep infections or abscess using labeled leukocytes.

  20. Polymorphisms of ICAM-1 are associated with gastric cancer risk and prognosis

    Institute of Scientific and Technical Information of China (English)

    Meng-Meng Tian; Yu Sun; Zhong-Wu Li; Ying Wu; Ai-Lian Zhao; Ji-You Li

    2012-01-01

    AIM: To investigate the association between single nucleotide polymorphisms (SNPs) in intercellular adhesion molecule-1 (ICAM-1) and the risk, biological behavior and prognosis of gastric cancer (GC) in Chinese population. METHODS: The study group consisted of 332 GC patients and 380 healthy controls. Genotyping was performed using polymerase chain reaction and the results were confirmed by sequencing. The association of ICAM-1 K469E polymorphisms and the risk of GC were studied, and the correlation of ICAM-1 K469E polymorphisms with the clinicopathological parameters and prognosis of the patients with complete clinical and follow-up data was analyzed.RESULTS: Carriers of AA genotype had a significantly increased risk of GC compared with carriers of AG and GG genotypes [odds ratios: 1.36; 95% confidence interval (CI): 1.01-1.84; P = 0.041]. GC patients with AA genotype were more prone to distant metastasis than those carrying AG and GG genotypes (18.9% vs 7.0%, respectively; P = 0.002). In addition, patients at stage Ⅳ had significantly more carriers of AA genotype than those of AG and GG genotype (27.4% vs 16.9%, respectively; P = 0.046). Follow-up study showed that the overall cumulative survival rate was 23.7% in AA genotype group and 42.9% in AG and GG genotypes group. In univariate analysis, AA genotype was correlated with the overall cumulative survival (P = 0.034). But in multivariate analysis, ICAM-1 polymorphism was not an independent prognostic factor for the overall survival (relative risk, 1.145; 95% CI: 0.851-1.540; P = 0.370). CONCLUSION: Polymorphisms of ICAM-1 K469E can be a useful biomarker for identifying individuals with higher risk of GC, predicting disease progression, and guiding individualized treatment.

  1. Expression of ICAM-1 and acute inflammatory cell infiltration in the early phase of radiation colitis in rats

    Energy Technology Data Exchange (ETDEWEB)

    Ikeda, Yuji; Ito, Masahiro; Matsuu, Mutsumi; Shichijo, Kazuko; Fukuda, Eiichiro; Nakayama, Toshiyuki; Nakashima, Masahiro; Naito, Shinji; Sekine, Ichiro [Nagasaki Univ. (Japan). Atomic Bomb Disease Inst.

    2000-09-01

    Inflammatory cell infiltration of the colon is observed at an early stage of radiation-induced colitis. The emigration of inflammatory cells from the circulation requires interactions between cell adhesion molecules on the vascular endothelium and molecules on the surface of leukocytes. To elucidate this process, the present work analyzes the kinetics of the expression of intercellular adhesion molecule-1 (ICAM-1) and the accumulation of inflammatory myeloperoxidase (MPO)-positive cells in relation to the appearance of acute radiation colitis prior to an overt radiation-induced ulcer. Colon tissues were obtained from Wistar Kyoto rats at various times after 22.5 Gy irradiation to the rectum. Histologically, crypt depletion and numerous inflammatory cells were observed 4 days after irradiation, and mucosal ulcer 6 days after irradiation. ICAM-1 immunopositivity was present in the endothelial cells of small vessels in the mucosa of both control and irradiated rats. ICAM-1 mRNA expression was detected in normal colon and irradiated colon by reverse transcription-PCR. In Northern blotting, ICAM-1 mRNA levels were found to increase markedly in the irradiated colon compared to the normal colon. In Western blotting, ICAM-1 protein expression also increased with a peak one day after irradiation, and remained elevated up to 6 days thereafter. The number of MPO-positive cells in lamina propria mucosa increased in a time-dependent fashion from 6 h to 6 days after irradiation. These data suggest that up-regulation of ICAM-1 in endothelial cells and accumulation of MPO positive cells play important roles in the development of radiation-induced colonic ulcer. (author)

  2. Psychological stress increases expression of aortic plaque intercellular adhesion molecule-1 and serum inflammatory cytokines in atherosclerotic rabbit model

    Institute of Scientific and Technical Information of China (English)

    Muwei Li; Xianpei Wang; Lei Yang; Chuanyu Gao; Yexin Ma

    2008-01-01

    Plaque rupture,platelet aggregation,and thrombogenesis are the main mechanisms of acute coronary syndrome (ACS),and inflammation factors play key roles in plaque unstability.Psychological stress promotes acute inflammatory response,leading to increased circulating levels of C-reactive protein (CRP),IL-6,and serum intercellular adhesion molecule (sICAM)-1.But it is not clear that whether psychological stress has a direct effect on atherosclerotic plaque stability.The purpose of this study was to investigate effects of chronic psychological stress on inflammatory marker (ICAM-1 ) in atherosclerotic plaque,and inflammatory markers in peripheral blood.Materials and methods Sixty male rabbits were randomized into 2 groups:the control group (n =10) and the atherosclerotic group (n =50).The latter were fed on high fatty diet and were given a large dose of vitamin D3 (3 600 000IU/kg) via intraperitoneal injection.After 8 weeks,the atherosclerotic model was estaslished.Then the 50 atherosclerotic model rabbits were divided into 3 subgroups:no-stress subgroup (n = 16),physiological stress subgroup (n = 16) and psychological stress subgroup (n =18).In physiological stress subgroup and psychological stress subgroup,drinking was cut from twice a day to once a day.At the same time,psychological stress subgroup was given empty bottle stress,and this process lasted for 2 weeks.One hour after the last stress,the blood samples were collected and the serum levels of CRP,IL-6 amd ICAM-1 were tested by radioimmunoassay or enzyme linked immunosorbent assay.The aorta and heart were extracted for pathology examination,and the express of ICAM-1 was tested by immunohistochemical examination.Results (1) After effective atherosclerotic animal model construction,the expression of ICAM-1 in aorta was higher in atherosclerotic group than that in control group (P<0.01),and was notably higher in psychological stress subgroup than that in no-stress subgroup or in physiological stress subgroup (2

  3. ICAM-1编码基因对乙型脑炎DNA疫苗树突状细胞功能的影响%Effect of ICAM-1 genetic adjuvant on dendritic cell function of plasmid DNA encoding prME protein derived from Japanese enaphalitis virus

    Institute of Scientific and Technical Information of China (English)

    翟永贞; 马力; 冯国和

    2013-01-01

    目的:研究细胞间粘附分子1(ICAM-1)编码基因对日本脑炎(JE) DNA疫苗脾脏树突状细胞功能的影响.方法:套式RT-PCR法获取BALB/c鼠ICAM-1编码基因,构建重组子pJME/ICAM-1和pICAM-1,脂质体法转染上述质粒于CHO细胞,Western blot法检测转染的CHO细胞中目的蛋白表达.实验分5组,包括:pJME/ICAM-1、pJME+ PICAM-1、pJME、JE灭活疫苗和pcDNA3.1(+)免疫组,以不同免疫原肌注免疫BALB/c小鼠,流式细胞仪检测经不同免疫原免疫鼠后脾脏DC表型、抗原吞噬功能以及混合淋巴细胞反应.结果:融合表达重组质粒pJME/ICAM-1和单质粒pICAM-1经鉴定构建正确.pJME/ICAM-1组CD11c+CD86+ DC和CD11c+ICAM-1+ DC比例分别为(6.92±1.40)%、(7.18±0.57)%,高于其它免疫组(均P<0.05);pJME/ICAM-1和pJME+ pICAM-1组DC表面CD80和MHCⅡ表达水平比较差异无统计学意义(P>0.05);pJME/ICAM-1与pJME+ pICAM-1组内吞能力明显增强,平均荧光强度分别为437.11 ±47.60、416.67±29.12,显著高于其它组(P<0.05).比较不同免疫原对细胞分裂的作用,以pJME/ICAM-1组最强,(73.69±7.32)% CD4+T细胞发生分裂,(45.40 ±2.57)%CD8 +T细胞发生分裂,显著高于对照组(P<0.05).结论:ICAM-1编码基因能够促进JE DNA疫苗脾脏树突状细胞的成熟,能够提供独立或放大B7分子的协同刺激信号.%Objective: To study the effect of intercellular adhesion molecule-1 (ICAM-1)coding gene on dendritic cell function induced by Japanese encephalitis (JE) virus DNA vaccine. Methods: ICAM-1 coding gene was amplified by nested-reverse tran-scriptase-polymerase chain reaction(RT-PCR) technique from BALB/c murine lung tissue. Recombinant plasmids pJME/ICAM-1 and pICAM-1 were constructed by JE virus ( JEV) prM-E protein with ICAM-1 coding gene or ICAM-1 coding gene only, respectively. The plasmids were transfected into China hamster ovary ( CHO) cells by Iipofectamine2000. The coding protein expressions was analyzed by Western blot

  4. SIRT1在内皮细胞中抑制PMA和ionomycin诱导的ICAM-1的表达%SIRT1 suppresses PMA and ionomycin-induced ICAM-1 expression in endothelial cells

    Institute of Scientific and Technical Information of China (English)

    贾玉艳; 高鹏; 陈厚早; 万言珍; 张然; 张祝琴; 杨瑞锋; 王旭; 徐静

    2013-01-01

    白细胞在内皮中的富集能够引起炎症并触发动脉粥样硬化,intercellular adhesion molecule-1 (ICAM-1)在该过程中发挥了重要作用.本实验室先前研究显示,内皮特异过表达Ⅲ类组蛋白去乙酰化酶SIRT1能够抑制动脉粥样硬化.因此,提出这样的假设:SIRT1能够抑制内皮细胞中ICAM-1的表达.实验发现,PMA和ionomycin(PMA/Io)能够在人脐静脉内皮细胞(HUVECs)中明显诱导SIRT1和ICAM-1的表达.而且,腺病毒介导的SIRT1过表达在HUVECs中能显著抑制PMA/Io诱导的ICAM-1的表达,而敲低SIRT1的表达则导致ICAM-1表达上调.双荧光素酶报告基因分析表明,过表达SIRT1抑制基础水平和PMA/Io诱导下的ICAM-1的启动子活性.进一步通过染色质免疫共沉淀(ChIP)实验发现,SIRT1参与转录复合物结合在ICAM-1启动子区,而且SIRT1的干扰能够提高NF-κB的亚基p65结合到ICAM-1启动子区的能力.总之,这些数据提示,SIRT1在内皮细胞中抑制ICAM-1表达的作用可能有助于其对抗动脉粥样硬化的发生.

  5. Novel association of ABO histo-blood group antigen with soluble ICAM-1: results of a genome-wide association study of 6,578 women.

    Directory of Open Access Journals (Sweden)

    Guillaume Paré

    2008-07-01

    Full Text Available While circulating levels of soluble Intercellular Adhesion Molecule 1 (sICAM-1 have been associated with diverse conditions including myocardial infarction, stroke, malaria, and diabetes, comprehensive analysis of the common genetic determinants of sICAM-1 is not available. In a genome-wide association study conducted among 6,578 participants in the Women's Genome Health Study, we find that three SNPs at the ICAM1 (19p13.2 locus (rs1799969, rs5498 and rs281437 are non-redundantly associated with plasma sICAM-1 concentrations at a genome-wide significance level (P<5x10(-8, thus extending prior results from linkage and candidate gene studies. We also find that a single SNP (rs507666, P = 5.1x10(-29 at the ABO (9q34.2 locus is highly correlated with sICAM-1 concentrations. The novel association at the ABO locus provides evidence for a previously unknown regulatory role of histo-blood group antigens in inflammatory adhesion processes.

  6. NDRG2 Expression Decreases Tumor-Induced Osteoclast Differentiation by Down-regulating ICAM1 in Breast Cancer Cells.

    Science.gov (United States)

    Kim, Bomi; Nam, Sorim; Lim, Ji Hyun; Lim, Jong-Seok

    2016-01-01

    Bone matrix is properly maintained by osteoclasts and osteoblasts. In the tumor microenvironment, osteoclasts are increasingly differentiated by the various ligands and cytokines secreted from the metastasized cancer cells at the bone metastasis niche. The activated osteoclasts generate osteolytic lesions. For this reason, studies focusing on the differentiation of osteoclasts are important to reduce bone destruction by tumor metastasis. The N-myc downstream-regulated gene 2 (NDRG2) has been known to contribute to the suppression of tumor growth and metastasis, but the precise role of NDRG2 in osteoclast differentiation induced by cancer cells has not been elucidated. In this study, we demonstrate that NDRG2 expression in breast cancer cells has an inhibitory effect on osteoclast differentiation. RAW 264.7 cells, which are monocytic preosteoclast cells, treated with the conditioned media (CM) of murine breast cancer cells (4T1) expressing NDRG2 are less differentiated into the multinucleated osteoclast-like cells than those treated with the CM of 4T1-WT or 4T1-mock cells. Interestingly, 4T1 cells stably expressing NDRG2 showed a decreased mRNA and protein level of intercellular adhesion molecule 1 (ICAM1), which is known to enhance osteoclast maturation. Osteoclast differentiation was also reduced by ICAM1 knockdown in 4T1 cells. In addition, blocking the interaction between soluble ICAM1 and ICAM1 receptors significantly decreased osteoclastogenesis of RAW 264.7 cells in the tumor environment. Collectively, these results suggest that the reduction of ICAM1 expression by NDRG2 in breast cancer cells decreases osteoclast differentiation, and demonstrate that excessive bone resorption could be inhibited via ICAM1 down-regulation by NDRG2 expression.

  7. Astragalus polysaccharides suppress ICAM-1 and VCAM-1 expression in TNF-α-treated human vascular endothelial cells by blocking NF-KB activation

    Institute of Scientific and Technical Information of China (English)

    Yu-ping ZHU; Tao SHEN; Ya-jun LIN; Bei-dong CHEN; Yang RUAN; Yuan CAO; Yue QIAO

    2013-01-01

    Aim:To investigate the effects ofAstragalus polysaccharides (APS) on tumor necrosis factor (TNF)-α-induced inflammatory reactions in human umbilical vein endothelial cells (HUVECs) and to elucidate the underlying mechanisms.Methods:HUVECs were treated with TNF-α for 24 h.The amounts of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1(VCAM-1) were determined with Western blotting.HUVEC viability and apoptosis were detected using cell viability assay and Hoechst staining,respectively.Reactive oxygen species (ROS) production was measured by DHE staining.Monocyte and HUVEC adhesion assay was used to detect endothelial cell adhesive function.NF-KB activation was detected with immunofluorescence.Results:TNF-α (1-80 ng/mL) caused dose-and time-dependent increases of ICAM-1 and VCAM-1 expression in HUVECs,accompanied by significant augmentation of IKB phosphorylation and NF-KB translocation into the nuclei.Pretreatment with APS (10 and 50 μg/mL)significantly attenuated TNFα-induced upregulation of ICAM-1,VCAM-1,and NF-KB translocation.Moreover,APS significantly reduced apoptosis,ROS generation and adhesion function damage in TNF-α-treated HUVECs.Conclusion:APS suppresses TNFα-induced adhesion molecule expression by blocking NF-KB signaling and inhibiting ROS generation in HUVECs.The results suggest that APS may be used to treat and prevent endothelial cell injury-related diseases.

  8. CXCL1-Triggered Interaction of LFA1 and ICAM1 Control Glucose-Induced Leukocyte Recruitment during Inflammation In Vivo

    Directory of Open Access Journals (Sweden)

    Kirsten Buschmann

    2012-01-01

    Full Text Available It is well acknowledged that proinflammatory stimulation during acute hyperglycemia is able to aggravate inflammatory diseases. However, the mechanisms of proinflammatory effects of glucose are controversially discussed. We investigated leukocyte recruitment after intravenous injection of glucose in different inflammatory models using intravital microscopy. Flow chamber experiments, expression analysis, functional depletion, and knockout of key adhesion molecules gave mechanistic insight in involved pathways. We demonstrated that a single injection of glucose rapidly increased blood glucose levels in a dose-dependent manner. Notably, during tumor necrosis factor (TNF α-induced inflammation leukocyte recruitment was not further enhanced by glucose administration, whereas glucose injection profoundly augmented leukocyte adhesion and transmigration into inflamed tissue in the trauma model, indicating that proinflammatory properties of glucose are stimulus dependent. Experiments with functional or genetic inhibition of the chemokine receptor CXCR2, intercellular adhesion molecule 1 (ICAM1, and lymphocyte function antigen 1 (LFA1 suggest that keratino-derived-chemokine CXCL1-triggered interactions of ICAM1 and LFA1 are crucially involved in the trauma model of inflammation. The lacking effect of glucose on β2 integrin expression and on leukocyte adhesion in dynamic flow chamber experiments argues against leukocyte-driven underlying mechanisms and favours an endothelial pathway since endothelial ICAM1 expression was significantly upregulated in response to glucose.

  9. Icam-1 targeted nanogels loaded with dexamethasone alleviate pulmonary inflammation.

    Directory of Open Access Journals (Sweden)

    M Carme Coll Ferrer

    Full Text Available Lysozyme dextran nanogels (NG have great potential in vitro as a drug delivery platform, combining simple chemistry with rapid uptake and cargo release in target cells with "stealth" properties and low toxicity. In this work, we study for the first time the potential of targeted NG as a drug delivery platform in vivo to alleviate acute pulmonary inflammation in animal model of LPS-induced lung injury. NG are targeted to the endothelium via conjugation with an antibody (Ab directed to Intercellular Adhesion Molecule-1(ICAM-NG, whereas IgG conjugated NG (IgG-NG are used for control formulations. The amount of Ab conjugated to the NG and distribution in the body after intravenous (IV injection have been quantitatively analyzed using a tracer isotope-labeled [125I]IgG. As a proof of concept, Ab-NG are loaded with dexamethasone, an anti-inflammatory therapeutic, and the drug uptake and release kinetics are measured by HPLC. In vivo studies in mice showed that: i ICAM-NG accumulates in mouse lungs (∼120% ID/g vs ∼15% ID/g of IgG-NG; and, ii DEX encapsulated in ICAM-NG, but not in IgG-NG practically blocks LPS-induced overexpression of pro-inflammatory cell adhesion molecules including ICAM-1 in the pulmonary inflammation.

  10. 清肺口服液对呼吸道合胞病毒肺炎患儿血清IL-8、ICAM-1表达水平的影响%Influence of Qingfei Oral Liquid on Expressions of Serum IL-8 and ICAM-1 in Children with Respiratory Syncytial Viral Pneumonia

    Institute of Scientific and Technical Information of China (English)

    袁斌; 王爱华; 徐建亚; 朱越; 李琳

    2013-01-01

    Objective:To study the influence of Qingfei Oral Liquid on serum levels of Interleukin -8 (IL-8) and Intercellular adhesion molecule - 1 ( ICAM - 1) in children with respiratory syncytial viral pneumonia. Methods: Enzyme - linked immuno -sorbent assay was used to measure the levels of serum IL-8 and ICAM - 1 in 8 children with respiratory syncytial viral pneumonia before and after the treatment with Qingfei Oral Liquid. Results:The level of serum IL-8 was obviously decreased, while the level of serum ICAM - 1 was obviously increased compared with those before treatment with Qingfei Oral Liquid, and the difference had a statistical significance (P <0. 05). Conclusion: Qingfei Oral Liquid can make the level of serum IL-8 lower and that of ICAM - 1 higher in 8 children with respiratory syncytial viral pneumonia.%目的:探讨清肺口服液对呼吸道合胞病毒肺炎患儿血清白介素-8(IL-8)、细胞间黏附分子-1(ICAM-1)的影响.方法:采用酶联免疫吸附法(ELISA),测量8例RSV肺炎患儿治疗前后血清中IL-8、ICAM-1水平.结果:清肺口服液治疗后患儿血清中IL-8水平比治疗前显著下降,而血清中ICAM-1水平比治疗前显著升高,差异有统计学意义(P<0.05).结论:清肺口服液可显著降低RSV肺炎患儿血清中IL-8水平,升高ICAM-1水平,可能与清肺口服液的免疫调节作用有关.

  11. Platelet endothelial cell adhesion molecule-1 signaling inhibits the activation of human platelets

    OpenAIRE

    Cicmil, Milenko; Stevens, Jo; Leduc, Mireille; Bon, Cassian; Gibbins, Jonathan M.

    2002-01-01

    Platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) is a 130-kd transmembrane glycoprotein and a member of the growing family of receptors with immunoreceptor tyrosine-based inhibitory motifs (ITIMs). PECAM-1 is expressed on platelets, certain T cells, monocytes, neutrophils, and vascular endothelial cells and is involved in a range of cellular processes, though the role of PECAM-1 in platelets is unclear. Cross-linking of PECAM-1 results in phosphorylation of the ITIM allowing the r...

  12. Integrin engagement mediates tyrosine dephosphorylation on platelet-endothelial cell adhesion molecule 1.

    OpenAIRE

    Lu, T T; Yan, L G; Madri, J. A.

    1996-01-01

    Platelet-endothelial cell adhesion molecule 1 (PECAM-1, CD31) is a 130-kDa member of the immunoglobulin gene superfamily expressed on endothelial cells, platelets, neutrophils, and monocytes and plays a role during endothelial cell migration. Phosphoamino acid analysis and Western blot analysis with anti-phosphotyrosine antibody show that endothelial PECAM-1 is tyrosine-phosphorylated. Phosphorylation is decreased with endothelial cell migration on fibronectin and collagen and with cell sprea...

  13. 持续气道正压通气对阻塞性睡眠呼吸暂停综合征患者血ICAM-1的影响%Effect of continuous positive airway pressure on blood ICAM-1 in obstructive sleep apnea syndrome patients

    Institute of Scientific and Technical Information of China (English)

    刘远程; 刘毅; 钱效森; 李浩波; 魏棉

    2013-01-01

    目的 评价阻塞性睡眠呼吸暂停综合征(OSAS)血清细胞间黏附分子-1(ICAM-1)水平及持续气道正压通气治疗(CPAP)对OSAS患者血清ICAM-1水平的影响.方法 收集20例健康对照者及20例OSAS患者的临床资料,回顾性分析两组患者多导睡眠呼吸监测结果,比较两组血清ICAM-1水平的差异;比较持续气道正压通气治疗前后OSAS患者血清ICAM-1水平的差异.结果 OSAS组患者治疗前血清ICAM-1含量为(105.26±37.470)μg/L,健康对照组血清ICAM-1含量为(99.98±18.78)μg/L,两组比较差异有统计学意义,P=0.018.经过CPAP治疗3个月后,OSAS组患者血清ICAM-1水平降至(93.34±21.24)μg/L,与治疗前血清ICAM-1水平比较,两组差异有统计学意义,P=0.037.结论 OSAS患者血清ICAM-1水平升高,持续气道正压通气治疗可有效降低OSAS患者血清ICAM-1水平.%Objective To analyze the influence of continuous positive airway pressure(CPAP) on serum intercellular adhesion molecule-1 (ICAM-1) in patients with obstructive sleep apnea syndrome(OSAS).Methods Clinical data and PSG results were collected in 20 patients with OSAS and 20 healthy subjects.Serum ICAM-1 level in all subjects were detected by ELISA method.Results Serum ICAM-1 content in OSAS patients was(105.26±37.47)μg/L and in healthy controls was (99.98±18.78)μg/L.Serum levels of ICAM-1 between the two groups were significantly different(P = 0.018).After 3 months treatment of CPAP, serum ICAM-1 level in OSAS patients fell to (93.34±21.24) μg/L, which was significantly different with that before treatment(P = 0.037).Conclusion Serum ICAM-1 content in OSAS patients might be greatly improved.CPAP treatment could effectively reduce serum ICAM-1 in OSAS patients.

  14. Hyperketonemia increases monocyte adhesion to endothelial cells and is mediated by LFA-1 expression in monocytes and ICAM-1 expression in endothelial cells

    OpenAIRE

    Rains, Justin L.; Jain, Sushil K.

    2011-01-01

    Frequent episodes of hyperketonemia are associated with a higher incidence of vascular disease. The objective of this study was to examine the hypothesis that hyperketonemia increases monocyte-endothelial cell (EC) adhesion and the development of vascular disease in diabetes. Human U937 and THP-1 monocyte cell lines and human umbilical vein endothelial cells (HUVECs) were cultured with acetoacetate (AA) (0–10 mM) or β-hydroxybutyrate (BHB) (0–10 mM) for 24 h prior to evaluating adhesion and a...

  15. P-Selectin Cross-Links PSGL-1 and Enhances Neutrophil Adhesion to Fibrinogen and ICAM-1 in a Src Kinase-Dependent, but GPCR-Independent Mechanism

    OpenAIRE

    Xu, Tao; Zhang, Lei; Geng, Zhen H; Wang, Hai-Bo; Wang, Jin-Tao; Chen, Ming; Geng, Jian-Guo

    2007-01-01

    Endothelial and platelet P-selectin (CD62P) and leukocyte integrin αMβ2 (CD11bCD18, Mac-1) are cell adhesion molecules essential for host defense and innate immunity. Upon inflammatory challenges, P-selectin binds to PSGL-1 (P-selectin glycoprotein ligand-1, CD162) to mediate neutrophil rolling, during which integrins become activated by extracellular stimuli for their firm adhesion in a G-protein coupled receptor (GPCR)-dependent mechanism. Here we show that cross-linking of PSGL-1 by dimeri...

  16. Fumaric Acid Esters Do Not Reduce Inflammatory NF-κB/p65 Nuclear Translocation, ICAM-1 Expression and T-Cell Adhesiveness of Human Brain Microvascular Endothelial Cells

    Directory of Open Access Journals (Sweden)

    Axel Haarmann

    2015-08-01

    Full Text Available Dimethyl fumarate (DMF is approved for disease-modifying treatment of patients with relapsing-remitting multiple sclerosis. Animal experiments suggested that part of its therapeutic effect is due to a reduction of T-cell infiltration of the central nervous system (CNS by uncertain mechanisms. Here we evaluated whether DMF and its primary metabolite monomethyl fumarate (MMF modulate pro-inflammatory intracellular signaling and T-cell adhesiveness of nonimmortalized single donor human brain microvascular endothelial cells at low passages. Neither DMF nor MMF at concentrations of 10 or 50 µM blocked the IL-1β-induced nuclear translocation of NF-κB/p65, whereas the higher concentration of DMF inhibited the nuclear entry of p65 in human umbilical vein endothelium cultured in parallel. DMF and MMF also did not alter the IL-1β-stimulated activation of p38 MAPK in brain endothelium. Furthermore, neither DMF nor MMF reduced the basal or IL-1β-inducible expression of ICAM-1. In accordance, both fumaric acid esters did not reduce the adhesion of activated Jurkat T cells to brain endothelium under basal or inflammatory conditions. Therefore, brain endothelial cells probably do not directly mediate a potential blocking effect of fumaric acid esters on the inflammatory infiltration of the CNS by T cells.

  17. Association of serum soluble intercellular cell adhesion molecule-1, soluble vascular cell adhesion molecule-1 and hypersensitivity-CRP levels with peripheral vascular disease of lower limbs in patients with type 2 diabetes mellitus%2型糖尿病患者血清可溶性细胞间和血管细胞黏附分子1及CRP与下肢血管病变的关系

    Institute of Scientific and Technical Information of China (English)

    谭擎缨; 王静; 阮芸; 阮勇; 王秀景; 姚佳琦; 姚乐燕

    2013-01-01

    Objective To investigate the association of serum levels of soluble intercellular cell adhesion molecule-1 (sICAM-1),soluble vascular cell adhesion molecule-1 (sVCAM-1) and high sensitivity C-reactive protein (hs-CRP) with peripheral vascular disease of lower limbs in patients with type 2 diabetes mellitus (T2DM).Methods One hundred and thirty T2DM patients admitted from October 2011 to October 2012,and 30 age/sex-matched healthy subjects were enrolled in the study.The serum levels of sICAM-1,sVCAM-1,hs-CRP and other clinical parameters were measured; the peripheral blood vessels of lower limbs were examined with color Doppler ultrasonography.Based on the extent of angiopathy of lower limbs T2DM patients were classified as normal vascular group (n =26),mild angiopathy group (n =45),moderate/severe angiopathy group (n =59).Results The serum levels of sICAM-1 and sVCAM-1 in moderate/ severe angiopathy group of T2DM patients were higher than those in mild angiopathy group,normal vascular group and healthy controls (t:4.15-8.93,all P <0.05) ; the serum levels of hs-CRP in moderate/severe angiopathy group were higher than those in mild angiopathy group,normal vascular group and healthy controls (t:2.18-4.27,all P < 0.05).The serum sICAM-1 level was positively correlated with total cholesterol (TC),low density lipoprotein cholesterol (LDL-C) and sVCAM-1.The serum sVCAM-1 level was positively correlated with course of disease,systolic blood pressure and CRP.Conclusions Serum levels of sICAM-1,sVCAM-1 and hs-CRP are correlated with the extent of angiopathy of lower limbs in T2DM patients,and the elevated sICAM-1 ; sVCAM-1 and hs-CRP levels are also associated with hyper blood pressure,dislipidemia and chronic inflammation.%目的 探讨2型糖尿病患者血清可溶性细胞间黏附分子1(sICAM-1)、血管细胞黏附分子1(sVCAM-1)及高敏CRP(hsCRP)水平与下肢大血管病变程度的关系.方法 对130例2型糖尿病患者(糖尿病组)与30例年龄匹配

  18. Inside-Out Regulation of ICAM-1 Dynamics in TNF-alpha-Activated Endothelium

    NARCIS (Netherlands)

    J.D. van Buul; J. van Rijssel; F.P.J. van Alphen; M. Hoogenboezem; S. Tol; K.A. Hoeben; J. van Marle; E.P.J. Mul; P.L. Hordijk

    2010-01-01

    Background: During transendothelial migration, leukocytes use adhesion molecules, such as ICAM-1, to adhere to the endothelium. ICAM-1 is a dynamic molecule that is localized in the apical membrane of the endothelium and clusters upon binding to leukocytes. However, not much is known about the regul

  19. Post-transcriptional down regulation of ICAM-1 in feto-placental endothelium in GDM.

    Science.gov (United States)

    Díaz-Pérez, Francisca Isidora; Hiden, Ursula; Gauster, Martin; Lang, Ingrid; Konya, Viktoria; Heinemann, Akos; Lögl, Jelena; Saffery, Richard; Desoye, Gernot; Cvitic, Silvija

    2016-03-01

    Maternal gestational diabetes (GDM) is associated with hyperglycaemia and hyperinsulinemia in the fetal circulation which consequently may induce endothelial dysfunction in the feto-placental vasculature. In fact, feto-placental vasculature reveals various morphological changes in response to GDM. The cell adhesion molecules (CAMs) ICAM-1, VCAM-1 and E-selectin promote attachment and trans-endothelial migration of leukocytes, and are up regulated in inflammation and endothelial dysfunction. Thus, we hypothesized that the GDM environment upregulates ICAM-1, VCAM-1 and E-selectin in the feto-placental endothelium. We isolated primary feto-placental endothelial cells (fpEC) after normal (n=18) and GDM pregnancy (n=11) and analyzed mRNA (RT-qPCR) and protein expression (Immunoblot) of ICAM-1, VCAM-1 and E-selectin. While other CAMs were unchanged on mRNA and protein levels, ICAM-1 protein was decreased by GDM. Further analysis revealed also a decrease in the release of soluble ICAM-1 (sICAM-1), whose levels correlated negatively with maternal BMI. We conclude that this reduction of ICAM-1 protein species is the result of post-translational regulation, since ICAM-1 mRNA expression was unchanged. In fact, miRNAs targeting ICAM-1 were upregulated in GDM fpEC. Immunohistochemistry showed weaker ICAM-1 staining in the placental endothelium after GDM pregnancies, and demonstrated ICAM-1 binding partners CD11a and CD18 expressed on leukocytes in fetal circulation and on placental tissue macrophages. This study identified reduction of ICAM-1 protein in fpEC in GDM pregnancy, which was regulated post-transcriptionally. Low ICAM-1 protein production may represent a protective, placenta-specific mechanism to avoid leukocyte transmigration into the placenta in response to GDM. PMID:26761204

  20. Role of ICAM-1 and E-selectin gene polymorphisms in pathogenesis of PAOD in Egyptian patients

    Directory of Open Access Journals (Sweden)

    Olfat Shaker

    2009-12-01

    Full Text Available Olfat Shaker1, Amr Zahra2, Ahmed Sayed3, Ayman Refaat4, Zakaria El-Khaiat5, Gehan Hegazy5, Khaled El-Hindawi3, Mohamed Ay-El Deen31Department of Medical Biochemistry, 3Vascular Surgery, Faculty of Medicine, Cairo University, Cairo, Egypt; 2Department of Medical Biochemistry, Faculty of Medicine, Fayoum University, Al Fayyum, Egypt; 4Vasular Surgery, Faculty of Medicine, Beni Suef University, Beni-Suef, Egypt; 5Medical Biochemistry Department, National Research Center, Cairo, EgyptBackground: Intercellular adhesion molecule-1 (ICAM-1 and E-selectin have been shown to predict cardiovascular disease (CVD such as myocardial infarction, stroke, and peripheral arterial occlusive disease (PAOD.Methods: Two mutations, S128R in E-selectin and K469E in ICAM-1, were investigated in 156 patients with PAOD and 100 control subjects using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP analysis in an Egyptian population.Results: The distribution of E-selectin genotypes in patients affected by PAOD was 84.6% for the AA genotype and 15.4% for the AC genotype. In the control arm the distribution was 97% for the AA genotype and 3% for the AC genotype. There was a statistically significance difference in the distribution of the AC genotype in PAOD patients when compared with the control subjects. Additionally, the distribution of ICAM-1 genotypes in patients affected by PAOD was 30.8% with the EE, 48% with the EK, and 21.2% with the KK genotypes. The distribution of ICAM-1 genotypes in control subjects was 13% EE, 33% EK and 54% KK. The EE genotype was significantly more common in PAOD patients than in the controls.Conclusion: S128R and K469E polymorphisms were associated with increased risk in PAOD. Early detection of these polymorphic genes helps in early prophylaxis against PAOD.Keywords: polymorphism, PAOD, E-selectin, ICAM-1, RFLP, genotyping

  1. Cell adhesion molecules and hyaluronic acid as markers of inflammation, fibrosis and response to antiviral therapy in chronic hepatitis C patients

    Directory of Open Access Journals (Sweden)

    Esther Granot

    2001-01-01

    Full Text Available Objective: Cell adhesion molecules (intracellular adhesion molecule-1 (ICAM-1, vascular cell adhesion molecule-1 (VCAM-1 and hyaluronic acid, markers of inflammation and fibrosis were monitored in hepatitis C patients to determine whether changes in plasma levels, during antiviral treatment, can predict long-term response to therapy.

  2. 反义寡核苷酸抑制缺氧/再给氧时内皮细胞细胞间粘附分子-1的表达%Inhibition of ICAM- 1 expression on endothelial cells inhypoxia/reoxygenation by antisense oligodeoxynucleotides

    Institute of Scientific and Technical Information of China (English)

    夏斌; 徐洪实; 邵福源; 陈蕾

    2000-01-01

    目的:探讨反义寡核苷酸(As-0DN)对缺氧/再给氧(H/R)时内皮细胞细胞间粘附分子-1(ICAM-1)表达的影响。方法:流式细胞仪测定肾小球血管内皮细胞在缺氧、再给氧及加入AS-0DN后ICAM-1表达的阳性百分率。结果:缺氧10 h,肾小球血管内皮细胞ICAM-1的表达与对照组无显著性差异,再给氧6 h ICAM-1的表达明显高于正常,加入As-ODN后,ICAM-1阳性细胞的百分率下降40.6%。结论:AS-ODN可以降低H/R时内皮细胞ICAM-1的表达。%AIM: To investigate the effect of antisense oligodeoxynucleotides (AS - ODN) on the intercellsular adhesion molecule- 1 (ICAM- 1 ) expression on endothelial cells in hypoxia/reoxygenation(H/R). METHODS: With cultured glomerular vascular endothelial cell in H/R, the positive percentage of ICAM - 1 expression was measured by flow cytometry before and after giving AS - ODN. RESULTS: The ICAM - 1 expression did not increase on glomerular vascular endothelial cell in 10 hours hypoxia compared to control group, it increased in 6 hours reoxygenation, and decreased by 40.6 % after giving AS- OND. CONCLUSION: AS - ODN may decrease the expression of ICAM- 1 on endothelial cells in H/R.

  3. Antidiabetic Rosiglitazone Reduces Soluble Intercellular Adhesion Molecule-1 Level in Type 2 Diabetic Patients with Coronary Artery Disease

    Directory of Open Access Journals (Sweden)

    Guang Wang

    2008-01-01

    Full Text Available Background. We investigated the level of soluble adhesion molecules in diabetic patients and the effect of the peroxisome proliferator-activated receptor-γ (PPAR-γ agonist rosiglitazone on plasma levels of adhesion molecules and an inflammation marker in type 2 diabetic patients with coronary artery disease (CAD after percutaneous coronary intervention (PCI. Methods. A total of 116 diabetic patients with CAD who had undergone PCI were randomized to receive rosiglitazone (4 mg/d or not for 6 months. Plasma levels of soluble intercellular adhesion molecules (sICAM-1 and P-selectin (sP-selectin were measured on ELISA. Results. After 6-month rosiglitazone treatment, plasma levels of sICAM-1 were lower than baseline and control group levels (370.4 (332.4–421.9 pg/mL versus 423.5 (327.4–500.3 pg/mL and 404.6 (345.2–483.4 pg/mL, P<.001. In addition, plasma levels of C-reactive protein were significantly reduced from baseline levels. However, plasma level of sP-selectin was not significantly lowered with rosiglitazone treatment than with control treatment after 6-month follow-up. Conclusions. Rosiglitazone reduces chronic inflammatory responses and improves levels of markers of endothelial dysfunction in patients with diabetes and CAD. PPAR-γ agonist may have a beneficial effect on the vascular endothelium through its anti-inflammatory mechanism and may be useful as therapy in patients undergoing PCI.

  4. 米诺地尔外用对化疗后小鼠ICAM-1和ELAM-1的影响%Effects of minoxidil on adhesion molecules ICAM-1 and ELAM-1 in serum and local follicules of C57BL/6 mice

    Institute of Scientific and Technical Information of China (English)

    邢飞; 姜波; 涂亚庭

    2010-01-01

    目的: 评价米诺地尔对小鼠血清和毛囊ICAM-1和ELAM-1水平的影响.方法: 环磷酰胺静脉注射建立C57BL/6小鼠化疗后脱发模型.米诺地尔酊涂抹小鼠背部皮肤后,切取皮肤标本观察毛囊组织学变化;应用ELISA法和免疫组化法检测小鼠血清及毛囊内ICAM-1和ELAM-1水平.结果: 小鼠于注射环磷酰胺后4天出现明显的弥漫性脱毛,组织学上毛囊多为退行期,米诺地尔组多为生长期毛囊.造模后小鼠血清ICAM-1和ELAM-1的水平分别为(46.57±10.25)ng/mL和(28.57±6.03)ng/mL,高于对照组(P<0.05);米诺地尔涂抹后血清ICAM-1和ELAM-1水平分别为(27.21±5.62)ng/mL和(17.21±4.80)ng/mL,明显低于模型组(P<0.05).结论: 米诺地尔可减缓环磷酰胺导致的生长期毛囊细胞凋亡和退行性变,并降低血清和毛囊局部ICAM-1和ELAM-1水平,对环磷酰胺所致的脱发有一定的防治作用.

  5. Tumour necrosis factor α enhances CCL2 and ICAM-1 expression in peripheral nerve microvascular endoneurial endothelial cells

    Directory of Open Access Journals (Sweden)

    Evan B. Stubbs

    2013-02-01

    Full Text Available Recruitment and trafficking of autoreactive leucocytes across the BNB (blood–nerve barrier is an early pathological insult in GBS (Guillain-Barré syndrome, an aggressive autoimmune disorder of the PNS (peripheral nervous system. Whereas the aetiology and pathogenesis of GBS remain unclear, pro-inflammatory cytokines, including TNFα (tumour necrosis factor α, are reported to be elevated early in the course of GBS and may initiate nerve injury by activating the BNB. Previously, we reported that disrupting leucocyte trafficking in vivo therapeutically attenuates the course of an established animal model of GBS. Here, PNMECs (peripheral nerve microvascular endothelial cells that form the BNB were harvested from rat sciatic nerves, immortalized by SV40 (simian virus 40 large T antigen transduction and subsequently challenged with TNFα. Relative changes in CCL2 (chemokine ligand 2 and ICAM-1 (intercellular adhesion molecule 1 expression were determined. We report that TNFα elicits marked dose- and time-dependent increases in CCL2 and ICAM-1 mRNA and protein content and promotes secretion of functional CCL2 from immortalized and primary PNMEC cultures. TNFα-mediated secretion of CCL2 promotes, in vitro, the transendothelial migration of CCR2-expressing THP-1 monocytes. Increased CCL2 and ICAM-1 expression in response to TNFα may facilitate recruitment and trafficking of autoreactive leucocytes across the BNB in autoimmune disorders, including GBS.

  6. Effect of combined Jiqi hypoglycemic tablet conventional western medicine treatment on plasma ET-1 and sICAM-1 levels in patients with DM2

    International Nuclear Information System (INIS)

    Objective: To investigate the clinical beneficial effect of Jiqi hypoglycemic tablet on lowering the plasma ET-1 and soluble intercellular adhesion molecule-1 (sICAM-1) levels in patients with DM2. Methods: Plasma ET-1 and sICAM-1 levels were determined with ELISA in 30 patients with DM2 randomly selected to be treated with conventional western only medicine and 30 other DM2 patients selected to be treated with additional Jiqi hypoglycemic tablet both before and after 3 months' treatment. The blood sugar level, HbAlc percentage and lipid test (cholesterol, triglyceride, HDL, LDL) were also examined. Results: Blood sugar levels decreased significantly after 3 months' treatment in both groups. However, favorable changes of levels of other parameters (HbAlc, TC, TG, HDL, LDL, ET-1, sICAM-1) were demonstrated only in the patients treated with combined Jiqi hypoglycemic tablet and conventional western medicine (P<0.05 or P<0.01). Conclusion: Additional Jiqi hypoglycemic tablet might be desirable for the treatment of DM2 patients, especially due to the possible protection on vascular endothelium through lowering of the plasma ET-1 and sICAM-1 levels. (authors)

  7. Increase in IL-6, TNF-a, and MMP-9, but not sICAM-1, concentrations depends on exercise duration

    DEFF Research Database (Denmark)

    Reihmane, Dace; Jurka, Antra; Tretjakovs, Peteris;

    2013-01-01

    ), tumour necrosis factor-α (TNF-α), soluble form of intercellular adhesion molecule-1 (sICAM-1), and matrix metalloproteinase-9 (MMP-9) was studied in 22 half-marathon (HM) and 18 marathon (M) male amateur runners who completed their exercise task in 1.8 ± 0.2 (mean ± standard deviation) and 3.6 ± 0.4 h...... ml−1; ∆TNF-α: 1.7 ± 1.9 vs. 0.5 ± 0.8 pg ml−1; MMP-9: 288 ± 216 vs. 145 ± 128 ng ml−1, respectively). sICAM-1 also increased with exercise, but similarly in M and HM (20 ± 40 vs. 23 ± 32 ng ml−1, respectively). Only sICAM-1 remained elevated 28 h post-exercise in both HM and M, while IL-6, TNF......-α, and MMP-9 returned to pre-exercise levels. Competitive HM and M races induce significant increases in IL-6, TNF-α, sICAM-1, and MMP-9 concentrations. As HM and M runners performed the competition with similar absolute intensity, the difference in response between the groups suggests that exercise duration...

  8. Association between functional variants of the ICAM1 and CRP genes and metabolic syndrome in Taiwanese subjects.

    Science.gov (United States)

    Hsu, Lung-An; Chang, Chi-Jen; Wu, Semon; Teng, Ming-Sheng; Chou, Hsin-Hua; Chang, Hsien-Hsun; Chang, Pi-Yueh; Ko, Yu-Lin

    2010-12-01

    Although inflammation has been shown to play an important role in metabolic syndrome (MetS), the association between inflammatory marker gene polymorphisms and the risk of MetS has not been fully elucidated. This study was initiated to investigate the association between functional variants of inflammatory marker genes and the risk of MetS in Taiwanese adults. The sample population comprised 615 unrelated subjects, of which 22% had MetS. The single nucleotide polymorphisms rs5491 on the intercellular adhesive molecule 1 (ICAM1) gene and rs3091244 on C-reactive protein (CRP) were genotyped. The ICAM1 rs5491 polymorphism was significantly associated with the level of soluble intercellular adhesive molecule 1 (P gene polymorphisms play an important role in modulating the risk of insulin resistance and MetS for subjects with central obesity. These findings will contribute toward a better understanding of the mechanism of association between inflammatory markers and the risk of developing atherosclerotic disease.

  9. Upregulation of Intercellular Adhesion Molecule 1 and Proinflammatory Cytokines by the Major Surface Proteins of Treponema maltophilum and Treponema lecithinolyticum, the Phylogenetic Group IV Oral Spirochetes Associated with Periodontitis and Endodontic Infections

    Science.gov (United States)

    Lee, Sung-Hoon; Kim, Kack-Kyun; Choi, Bong-Kyu

    2005-01-01

    Treponema maltophilum and Treponema lecithinolyticum belong to the group IV oral spirochetes and are associated with endodontic infections, as well as periodontitis. Recently, the genes encoding the major surface proteins (Msps) of these bacteria (MspA and MspTL, respectively) were cloned and sequenced. The amino acid sequences of these proteins showed significant similarity. In this study we analyzed the functional role of these homologous proteins in human monocytic THP-1 cells and primary cultured periodontal ligament (PDL) cells using recombinant proteins. The complete genes encoding MspA and MspTL without the signal sequence were cloned into Escherichia coli by using the expression vector pQE-30. Fusion proteins tagged with N-terminal hexahistidine (recombinant MspA [rMspA] and rMspTL) were obtained, and any possible contamination of the recombinant proteins with E. coli endotoxin was removed by using polymyxin B-agarose. Flow cytometry showed that rMspA and rMspTL upregulated the expression of intercellular adhesion molecule 1 (ICAM-1) in both THP-1 and PDL cells. Expression of proinflammatory cytokines, such as interleukin-6 (IL-6) and IL-8, was also induced significantly in both cell types by the Msps, as determined by reverse transcription-PCR and an enzyme-linked immunosorbent assay, whereas IL-1β synthesis could be detected only in the THP-1 cells. The upregulation of ICAM-1, IL-6, and IL-8 was completely inhibited by pretreating the cells with an NF-κB activation inhibitor, l-1-tosylamido-2-phenylethyl chloromethyl ketone. This suggests involvement of NF-κB activation. The increased ICAM-1 and IL-8 expression in the THP-1 cells obtained with rMsps was not inhibited in the presence of the IL-1 receptor antagonist (IL-1ra), a natural inhibitor of IL-1. Our results show that the Msps of the group IV oral spirochetes may play an important role in amplifying the local immune response by continuous inflammatory cell recruitment and retention at an

  10. Effect of Cell Adhesion Molecule 1 Expression on Intracellular Granule Movement in Pancreatic α Cells.

    Science.gov (United States)

    Yokawa, Satoru; Furuno, Tadahide; Suzuki, Takahiro; Inoh, Yoshikazu; Suzuki, Ryo; Hirashima, Naohide

    2016-09-01

    Although glucagon secreted from pancreatic α cells plays a role in increasing glucose concentrations in serum, the mechanism regulating glucagon secretion from α cells remains unclear. Cell adhesion molecule 1 (CADM1), identified as an adhesion molecule in α cells, has been reported not only to communicate among α cells and between nerve fibers, but also to prevent excessive glucagon secretion from α cells. Here, we investigated the effect of CADM1 expression on the movement of intracellular secretory granules in α cells because the granule transport is an important step in secretion. Spinning disk microscopic analysis showed that granules moved at a mean velocity of 0.236 ± 0.010 μm/s in the mouse α cell line αTC6 that expressed CADM1 endogenously. The mean velocity was significantly decreased in CADM1-knockdown (KD) cells (mean velocity: 0.190 ± 0.016 μm/s). The velocity of granule movement decreased greatly in αTC6 cells treated with the microtubule-depolymerizing reagent nocodazole, but not in αTC6 cells treated with the actin-depolymerizing reagent cytochalasin D. No difference in the mean velocity was observed between αTC6 and CADM1-KD cells treated with nocodazole. These results suggest that intracellular granules in pancreatic α cells move along the microtubule network, and that CADM1 influences their velocity. PMID:27262873

  11. The Correlation between Serum ICAM-1 and IL -6 Levels and the Degree of Renal Function Injury%血清ICAM-1和IL-6水平与肾功能损害的相关性研究

    Institute of Scientific and Technical Information of China (English)

    石海燕; 胡维维; 杨秀媚; 赖均鹏; 刘笑芬

    2013-01-01

    Objective:To investigate correlation of serum Intercellular adhesion molecule-1 and Interleukin-6 levels with renal injury, to reveal the clinical value of serum ICAM-1 and IL -6 concentration detection for evaluation of renal function injury.Method:48 subjects were collected, who received renal function injury evaluation from August 2011 to July 2012. ELISA was performed to detect serum ICAM-1 and IL -6 concentration,and semi automatic biochemical analyzer was used to measure serum creatinine concentration, which was used for calculation of glomerular filtration rate ( eGFR ) value. Compared serum ICAM-1 and IL -6 concentrations of subjects with eGFR≥ 90 and eGFR < 90 , and analyzed the correlation between serum ICAM-1 and IL -6 concentrations and eGFR value.Result:Serum ICAM-1 and interleukin -6 concentrations of eGFR < 90 group ( renal injury group ) were significantly higher than those of eGFR ≥ 90 group (normal renal function group ) (P<0.05).Serum ICAM-1 and IL -6 concentration and eGFR value of patients with eGFR < 90 were significantly negative correlation (r=-0.9283, P=-0.013; r=-0.9369,P=0.001).Conclusion:The serum ICAM-1 and interleukin -6 levels may correlate with the renal function injury development, and its concentration detection may have potential value for evaluating the degree of renal function injury.%  目的:探讨血清细胞间粘附分子-1和白细胞介素-6表达与肾功能损害的相关性,用以评价血清ICAM-1和IL-6浓度检测用于评价肾功能损伤中的临床价值。方法:选择2011年8月-2012年7月来本院接受肾功能损伤检查的48例患者为研究对象。采用ELISA检测血清ICAM-1和IL-6浓度,采用半自动生化分析仪检测血清肌酐浓度并计算肾小球滤过率(eGFR)值。比较eGFR≥90组和eGFR<90组血清ICAM-1和IL-6浓度,并分析血清ICAM-1和IL-6浓度与eGFR的相关性。结果:eGFR<90组(肾功能损伤组)血清ICAM-1和IL-6

  12. Ba-Wei-Di-Huang-Wan through its active ingredient loganin counteracts substance P-enhanced NF-κB/ICAM-1 signaling in rats with bladder hyperactivity.

    Science.gov (United States)

    Tsai, Wen-Hsin; Wu, Chung-Hsin; Cheng, Chen-Hung; Chien, Chiang-Ting

    2016-09-01

    Overt bladder afferent activation may exacerbate endogenous substance P (SP) release to induce intercellular adhesion molecule-1 (ICAM-1)-mediated inflammation and reactive oxygen species (ROS) production leading to hyperactive bladder. Ba-Wei-Die-Huang-Wan (BWDHW), a traditional Chinese medicine, has been used to treat lower urinary tract symptoms in patients by undefined mechanisms. We explored the possible mechanisms and the active components of BWDHW on exogenous SP-induced bladder hyperactivity. BWDHW contained six major components: loganin, paeoniflorin, 5-hydroxymethylfurfural, cinnamic acid, cinnamaldehyde, and paeonol by high-performance liquid chromatography. In urethane-anesthetized female Wistar rats, we evaluated transcystometrogram, pelvic afferent nerve activity by electrophysiologic recording techniques, ICAM-1 expression by Western blot and immunohistochemistry, ROS amount by an ultrasensitive chemiluminescence method and possible ROS sources from the different leukocytes by specific stains in SP-treated bladder. BWDHW and its major component loganin dose-dependently inhibited H2 O2 and HOCl activity in vitro. Intragastrical BWDHW (250 mg/kg) and loganin (5 mg/kg) twice daily for 2 weeks did not affect the baseline micturition parameters. Intra-arterial SP (20 µg/rat) through neurokinin-1 receptor activation increased voiding frequency (shortened intercontraction intervals), pelvic afferent nerve activity, bladder NF-κB/ICAM-1 expression, bladder ROS amount, neutrophils adhesion to venous endothelium, CD68 (monocyte/macrophage), and mast cell infiltration in the inflamed bladder. BWDHW and loganin pretreatment significantly depressed SP-enhanced pelvic afferent nerve activity, bladder NF-κB/ICAM-1 expression, leukocyte infiltration, and ROS amount, and subsequently improved bladder hyperactivity. In conclusion, our results suggest that BWDHW and its active component loganin improves bladder hyperactivity via inhibiting SP/neurokinin-1

  13. Relationship between the advanced glycation end products content and expressions of RAGE,ICAM-1 in vascular tissue of diabetic rats%糖尿病大鼠血管糖基化终产物含量与其受体和ICAM-1表达的关系

    Institute of Scientific and Technical Information of China (English)

    张建伟; 孙仁宇

    2001-01-01

    In this study,the relationship between the advanced glycation end products(AGEs) and the expressions of receptor for AGEs(RAGE),intercellular cell adhesion molecule-1(ICAM-1) was investigated.The diabetic rat model was reconstructed and the fluorescence method,RT-PCR and in-situ hybridization techniques were used to detect AGEs content and the expressions of RAGE and ICAM-1 gene in the aorta and cardiac tissues.The results showed that AGEs content in aortic and cardiac tissues increased(P<0.01) in diabetic rats; The expressions of RAGE and ICAM-1 enhanced (P<0.05~0.01) and were positively correlated with the quantity of AGEs accumulation(P<0.01) in the aorta and cardiac tissue.These parameters change in the diabetic rats can be improved with aminoglumine(AG) treatment.Suggesting that AGEs might induce RAGE and ICAM-1 expression.It's postulated that AGEs binding to RAGE play an important role to result in diabetic endothelial cells dysfunction and lesion.%探讨糖尿病大鼠血管组织糖基化终产物(AGEs)含量与其受体(RAGE)和细胞间粘附因子-1(ICAM-1)表达的关系。复制糖尿病大鼠模型,采用荧光法、RT-PCR及原位杂交方法检测主动脉及心肌组织的AGEs含量以及RAGE和ICAM-1基因的表达。发现糖尿病大鼠主动脉和心肌组织AGEs含量升高(P<0.01);RAGE和ICAM-1基因表达增强(P<0.05~0.01);AGEs含量与RAGE及ICAM-1呈明显正相关(P<0.01);氨基胍治疗可缓解上述指标的变化。提示AGEs可诱导RAGE和ICAM-1的表达。推测AGEs -RAGE相互作用是引起糖尿病血管内皮细胞功能紊乱和损伤的关键环节。

  14. Regulatory peptides modulate ICAM-1 gene expression and NF-κB activity in bronchial epithelial cells%肺内调节肽对支气管上皮细胞ICAM-1表达及NF-κB活性的调控

    Institute of Scientific and Technical Information of China (English)

    谭宇蓉; 秦晓群; 管茶香; 张长青; 罗自强; 孙秀泓

    2003-01-01

    细胞间粘附分子-1 (ICAM-1)是介导细胞与细胞之间粘附的重要生物分子; 核因子-κB (NF-κB)是体内普遍存在、能迅速对刺激产生反应的重要核转录因子.越来越多的证据显示, ICAM-1表达与NF-κB激活是炎症反应的重要步骤.我们应用免疫组化、RT-PCR、凝胶阻滞电泳(EMSA)等多种实验方法, 观察了肺内调节肽对支气管上皮细胞ICAM-1表达及NF-κB活性的影响, 以及NF-κB抑制剂MG-132对ICAM-1表达的影响.实验结果发现, VIP、EGF可使臭氧应激BECs的ICAM-1表达降低; ET-1、CGRP可使未受应激BECs的ICAM-1表达增加.NF-κB抑制剂MG-132可阻断O3、ET-1、CGRP引起的ICAM-1表达, 提示NF-κB在调控ICAM-1表达中起重要作用. EMSA结果显示, BECs中NF-κB在臭氧应激下反复激活,CGRP与ET-1可促进NF-κB的激活; VIP与EGF可抑制臭氧应激的BECs中NF-κB的激活.以上结果说明, VIP、EGF可通过下调ICAM-1转录及NF-κB激活减轻炎症反应, 而ET-1、CGRP可通过上调ICAM-1转录及NF-κB激活、加大炎症反应.ICAM-1与NF-κB的持续表达和反复激活是炎症持续加重发展的重要因素.%Intercellular adhesion molecule-1 (ICAM-1) is an important adhesion molecule leading to adhesion between cells; NF-ΚB, being universally distributed in the organism, is an important nuclear transcription factor leading to a rapid response to the stimuli. Line of evidence have shown that ICAM-1 transcription and NF-ΚB activation is an important step of inflammatory reaction. To testify that intrapulmonary regulatory peptides modulate inflammatory lesion of bronchial epithelial cells (BECs) through their effect on ICAM-1 expression and nuclear factor ΚB (NF-ΚB) activation, we used immunocytochemistry, RT-PCR, and electrophoretic mobility-shift assay (EMSA) to determine the ICAM-1 expression and NF-ΚB activity in BECs. The effects of NF-ΚB inhibitor MG-132 on ICAM-1 expression were also observed. The results showed that

  15. SIRT1在内皮细胞中抑制PMA和ionomycin诱导的ICAM-1的表达

    Institute of Scientific and Technical Information of China (English)

    贾玉艳; 高鹏; 陈厚早; 万言珍; 张然; 张祝琴; 杨瑞锋; 王旭; 徐静; 刘德培

    2013-01-01

    白细胞在内皮中的富集能够引起炎症并触发动脉粥样硬化,intercellular adhesion molecule-1ICAM-1)在该过程中发挥了重要作用.本实验室先前研究显示,内皮特异过表达Ⅲ类组蛋白去乙酰化酶SIRT1能够抑制动脉粥样硬化.因此,提出这样的假设:SIRT1能够抑制内皮细胞中ICAM-1的表达.实验发现,PMA和ionomycin(PMA/Io)能够在人脐静脉内皮细胞(HUVECs)中明显诱导SIRT1和ICAM-1的表达.而且,腺病毒介导的SIRT1过表达在HUVECs中能显著抑制PMA/Io诱导的ICAM-1的表达,而敲低SIRT1的表达则导致ICAM-1表达上调.双荧光素酶报告基因分析表明,过表达SIRT1抑制基础水平和PMA/Io诱导下的ICAM-1的启动子活性.进一步通过染色质免疫共沉淀(ChIP)实验发现,SIRT1参与转录复合物结合在ICAM-1启动子区,而且SIRT1的干扰能够提高NF-κB的亚基p65结合到ICAM-1启动子区的能力.总之,这些数据提示,SIRT1在内皮细胞中抑制ICAM-1表达的作用可能有助于其对抗动脉粥样硬化的发生.

  16. Edge restenosis: impact of low dose irradiation on cell proliferation and ICAM-1 expression

    Directory of Open Access Journals (Sweden)

    Hannekum Andreas

    2006-07-01

    Full Text Available Abstract Background Low dose irradiation (LDI of uninjured segments is the consequence of the suggestion of many authors to extend the irradiation area in vascular brachytherapy to minimize the edge effect. Atherosclerosis is a general disease and the uninjured segment close to the intervention area is often atherosclerotic as well, consisting of neointimal smooth muscle cells (SMC and quiescent monocytes (MC. The current study imitates this complex situation in vitro and investigates the effect of LDI on proliferation of SMC and expression of intercellular adhesion molecule-1 (ICAM-1 in MC. Methods Plaque tissue from advanced primary stenosing lesions of human coronary arteries (9 patients, age: 61 ± 7 years was extracted by local or extensive thrombendarterectomy. SMC were isolated and identified by positive reaction with smooth muscle α-actin. MC were isolated from buffy coat leukocytes using the MACS cell isolation kit. For identification of MC flow-cytometry analysis of FITC-conjugated CD68 and CD14 (FACScan was applied. SMC and MC were irradiated using megavoltage photon irradiation (CLINAC2300 C/D, VARIAN, USA of 6 mV at a focus-surface distance of 100 cm and a dose rate of 6 Gy min-1 with single doses of 1 Gy, 4 Gy, and 10 Gy. The effect on proliferation of SMC was analysed at day 10, 15, and 20. Secondly, total RNA of MC was isolated 1 h, 2 h, 3 h, and 4 h after irradiation and 5 μg of RNA was used in standard Northern blot analysis with ICAM-1 cDNA-probes. Results Both inhibitory and stimulatory effects were detected after irradiation of SMC with a dose of 1 Gy. At day 10 and 15 a significant antiproliferative effect was found; at day 20 after irradiation cell proliferation was significantly stimulated. Irradiation with 4 Gy and 10 Gy caused dose dependent inhibitory effects at day 10, 15, and 20. Expression of ICAM-1 in human MC was neihter inhibited nor stimulated by LDI. Conclusion Thus, the stimulatory effect of LDI on SMC

  17. 严重烧伤后早期大鼠肾脏细胞粘附分子1和白介素6的表达与肾功能损害的相关性研究%Expression of intercellular adhesion molecule 1 and interleukin 6 in the rat's kidney after severe burn and its relation with renal injury

    Institute of Scientific and Technical Information of China (English)

    刘开军; 魏敏; 刘杰; 鲁华玉; 王德文; 张燕

    2002-01-01

    Objective To clarify the mechanism and provide the basis for prevention and treatment of the early injuries of kidney after severe burn in rats.We observed the expression of intercellular adhesion molecule 1 and interleukin 6 and the early pathological changes in different time.Method Early pathological changes in the kidney were observed by LM and EM.The expression of ICAM 1 were observed by immunohistochemistry,in situ hybridization.The expression of IL 6 was also observed.Result From 5 min to 72 h after burn,the early changes in the kidney included edema,hemorrhage, and congestion,injury of capillary epithelium cells.2ICAM 1 and IL 6 were higher in the kidney 30 min after burn,and from 2 h to 24 h,they were strongest positive,but on 72 h,they were negative.Conclusion ICAM-1 and IL 6 may play important roles in mechanisms of kidney injury,and the major target cells may be the endothelium cells.

  18. 小儿体外循环手术围术期细胞间粘附分子-1的测定%Detection of Intercellular Adhesion Molecule-1 during Pediatric Cardiopulmonary Bypass

    Institute of Scientific and Technical Information of China (English)

    李建华; 张泽伟; 陈黎勤

    2000-01-01

    To evaluate the role of serum intercellular adhesion molecule (ICAM-1)changes during pediatric cardiopulmonary bypass (CPB) surgery for congenital heart diseases (CHD)and the clinic significance of monitoring the serum ICAM-1 level. Methods: ICAM-1 levels were measured by double antibodies sandwich ELISA in arterial specimen from 33 CPB cases at various time points,the results were compared with those of 10 non-CPB patients and 30 normal children. Results:Patients with CHD had normal levels of serum ICAM-1 before surgery. The serum ICAM-1 levels in CPB group were significantly higher than those of controls (P〈0. 005). ICAM-1 levels started increasing as early as 30 minutes of CPB began and peaked 24 hours after surgery and stayed up 48 hours after surgery . The serum ICAM-1 levels in patients whose CPB lasted longer than 90 minuets were significantly higher (P<0.05). Conclusion:ICAM-1 showed higher and lasted longer after pediatric CPB surgery. The length of CPB is associated with elevation of ICAM-1. Monitoring of serumICAM-1 ,in certain degree,may help in predicting prognosis and complication after CPB surgery.%目的:探讨小儿体外循环(CPB)围术期血清细胞间粘附分子-1(ICAM-1)水平变化规律和升高原因及测定的临床意义。方法:采用双抗夹心法酶联吸附试验(ELISA)法分别于手术前、转流后30 min、手术毕、术后2 h、12 h、24 h、48 h共7个时点测定33例先天性心脏病(CHD)患儿;分别于术前,术中及术后2 h测定10例非体外循环普胸手术患儿及30例健康体检患儿ICAM-1水平。结果:CHD术前ICAM-1无变化;CPB术后ICAM-1水平较非CPB明显升高,P<0.005;血清ICAM-1值于CPB 30 min后开始上升,至24 h达到高峰后开始下降,48 h尚未降至术前水平;CPB时间≥90 min组ICAM-1显著升高,P<0.05。结论:小儿CPB心脏直视手术后血清ICAM-1升高明显,CPB时间是ICAM-1升高的主要原因,ICAM-1测定对预防及早期发现并

  19. Increased plasma levels of soluble ICAM-1 and ELAM-1 (E-selectin) during acute Plasmodium falciparum malaria

    DEFF Research Database (Denmark)

    Hviid, L; Theander, T G; Elhassan, I M;

    1993-01-01

    ). In the present study we show that clinical episodes of P. falciparum malaria produced an increase in plasma levels of soluble ICAM-1 (sICAM-1) and ELAM-1 (sELAM-1). The increase was transient and subsided slowly (sICAM-1) or rapidly (sELAM-1) following drug cure. The increases in plasma sICAM-1 and sELAM-1 were...... significantly correlated, and were furthermore associated with a concomitant increase in plasma levels of sIL-2R. Finally, plasma levels of sICAM-1, but not sELAM-1, were inversely correlated to the fraction of peripheral T cells having high surface expression of LFA-1, the receptor for T-cell adhesion to ICAM......-1. Taken together, these observations suggest that acute P. falciparum malaria is characterized by a state of endothelial inflammation associated with the adherence of activated T cells....

  20. Effect of rosuvastatin on serum high-sensitive C-reactive protein and cell adhesion molecules-1 in elderly patients with primary hypertension%瑞舒伐他汀对老年原发性高血压患者超敏C反应蛋白和细胞间黏附分子-1的影响

    Institute of Scientific and Technical Information of China (English)

    谢文超; 李平; 陈坚; 林智海

    2013-01-01

    目的 探讨瑞舒伐他汀对老年原发性高血压患者超敏C反应蛋白(hs-CRP)和细胞间黏附分子-1(ICAM-1)的影响.方法 将44例患者随机分为常规治疗组和瑞舒伐他汀组.常规组采用氨氯地平治疗,如血压未达标则加用缬沙坦和比索洛尔至血压达标.治疗组在常规组治疗基础上加用瑞舒伐他汀片10 mg/d,连用4周.治疗前、后采用双抗体夹心ABC-ELISA法检测血清hs-CRP和ICAM-1浓度并进行统计学比较.结果 与治疗前相比,两组治疗后4周血清hs-CRP和ICAM-1水平显著下降,差异有统计学意义(P<0.01).治疗后4周,瑞舒伐他汀组的血清hs-CRP和ICAM-1水平比常规治疗组下降更多,差异有统计学意义(分别为t=2.1267,P=-0.0333; t=5.7905,P=-0.0000).结论 瑞舒伐他汀等他汀类药物可降低老年原发性高血压患者血清hs-CRP和ICAM-1等促炎性细胞因子的水平,减轻高血压患者的血管内炎症.%Objective To discussion the effect of rosuvastatin on serum high-sensitive C-reactive protein and cell adhesion molecules-1 in elderly patients with primary hypertension. Methods 44 elderly patients with primary hypertension were randomly divided into rosuvastatin group (n=22) and control group (n=22). Patients in control group were treated with amlodipine only or combine with valsartan bisoprolol together in order to control the blood pressure. Patients in rosuvastatin group were treated with rosuvastatin 10 mg/d base on the control group. Before and after rosuvastatin treatment, the serum high-sensitive C-reactive protein and cell adhesion molecules-1 level were measured, which were treated with group comparisons. Results The serum high-sensitive C-reactive protein and cell adhesion molecules-1 level both in control group and rosuvastatin group were decreased statistically after drug treatment. Compared with the control group, the serum high-sensitive C-reactive protein and cell adhesion molecules-1 level in rosuvastatin group were

  1. Matrine Attenuates COX-2 and ICAM-1 Expressions in Human Lung Epithelial Cells and Prevents Acute Lung Injury in LPS-Induced Mice

    Directory of Open Access Journals (Sweden)

    Chian-Jiun Liou

    2016-01-01

    Full Text Available Matrine is isolated from Sophora flavescens and shows anti-inflammatory effects in macrophages. Here we evaluated matrine’s suppressive effects on cyclooxygenase 2 (COX-2 and intercellular adhesion molecule-1 (ICAM-1 expressions in lipopolysaccharide- (LPS- stimulated human lung epithelial A549 cells. Additionally, BALB/c mice were given various matrine doses by intraperitoneal injection, and then lung injury was induced via intratracheal instillation of LPS. In LPS-stimulated A549 cells, matrine inhibited the productions of interleukin-8 (IL-8, monocyte chemotactic protein-1, and IL-6 and decreased COX-2 expression. Matrine treatment also decreased ICAM-1 protein expression and suppressed the adhesion of neutrophil-like cells to inflammatory A549 cells. In vitro results demonstrated that matrine significantly inhibited mitogen-activated protein kinase phosphorylation and decreased nuclear transcription factor kappa-B subunit p65 protein translocation into the nucleus. In vivo data indicated that matrine significantly inhibited neutrophil infiltration and suppressed productions of tumor necrosis factor-α and IL-6 in mouse bronchoalveolar lavage fluid and serum. Analysis of lung tissue showed that matrine decreased the gene expression of proinflammatory cytokines, chemokines, COX-2, and ICAM-1. Our findings suggest that matrine improved lung injury in mice and decreased the inflammatory response in human lung epithelial cells.

  2. Matrine Attenuates COX-2 and ICAM-1 Expressions in Human Lung Epithelial Cells and Prevents Acute Lung Injury in LPS-Induced Mice.

    Science.gov (United States)

    Liou, Chian-Jiun; Lai, You-Rong; Chen, Ya-Ling; Chang, Yi-Hsien; Li, Zih-Ying; Huang, Wen-Chung

    2016-01-01

    Matrine is isolated from Sophora flavescens and shows anti-inflammatory effects in macrophages. Here we evaluated matrine's suppressive effects on cyclooxygenase 2 (COX-2) and intercellular adhesion molecule-1 (ICAM-1) expressions in lipopolysaccharide- (LPS-) stimulated human lung epithelial A549 cells. Additionally, BALB/c mice were given various matrine doses by intraperitoneal injection, and then lung injury was induced via intratracheal instillation of LPS. In LPS-stimulated A549 cells, matrine inhibited the productions of interleukin-8 (IL-8), monocyte chemotactic protein-1, and IL-6 and decreased COX-2 expression. Matrine treatment also decreased ICAM-1 protein expression and suppressed the adhesion of neutrophil-like cells to inflammatory A549 cells. In vitro results demonstrated that matrine significantly inhibited mitogen-activated protein kinase phosphorylation and decreased nuclear transcription factor kappa-B subunit p65 protein translocation into the nucleus. In vivo data indicated that matrine significantly inhibited neutrophil infiltration and suppressed productions of tumor necrosis factor-α and IL-6 in mouse bronchoalveolar lavage fluid and serum. Analysis of lung tissue showed that matrine decreased the gene expression of proinflammatory cytokines, chemokines, COX-2, and ICAM-1. Our findings suggest that matrine improved lung injury in mice and decreased the inflammatory response in human lung epithelial cells.

  3. Conjugated linoleic acids suppress inflammatory response and ICAM-1 expression through inhibition of NF-κB and MAPK signaling in human bronchial epithelial cells.

    Science.gov (United States)

    Huang, Wen-Chung; Tu, Rong-Syuan; Chen, Ya-Ling; Tsai, Yun-Yun; Lin, Chwan-Fwu; Liou, Chian-Jiun

    2016-04-20

    Conjugated linoleic acids (CLAs) comprise a group of natural unsaturated fatty acids. CLA was reported to have anti-asthma, anti-adiposity, and anti-tumor effects. The present study aimed to evaluate the suppressive effects of cis-9, trans-11-CLA (c9,t11-CLA) on the expression of proinflammatory cytokines and intercellular adhesion molecule 1 (ICAM-1) in TNF-α-stimulated human bronchial epithelial (BEAS-2B) cells. After treating with various doses of c9,t11-CLA (12.5-100 μg ml(-1)), BEAS-2B cells were induced into an inflamed state by adding TNF-α or TNF-α/IL-4. The presence of c9,t11-CLA significantly suppressed the secretion of cytokines IL-6, IL-8, CCL5, and MCP-1. We also found that c9,t11-CLA inhibited ICAM-1 expression, and decreased monocyte adhesion to inflamed bronchial epithelial cells. Interestingly, c9,t11-CLA attenuated the phosphorylation of mitogen-activated protein kinase (MAPK) and down-regulated the activation of nuclear factor-κB (NF-κB). These results suggested that the anti-inflammatory effects of c9,t11-CLA were mediated by inhibiting proinflammatory cytokines, chemokines, and ICAM-1 expression by blocking NF-κB transcription regulation and by attenuating MAPK signaling pathways. PMID:27007063

  4. Dietary Antioxidants Decrease Serum Soluble Adhesion Molecule (sVCAM-1, sICAM-1 but not Chemokine (JE/MCP-1, KC Concentrations, and Reduce Atherosclerosis in C57BL but Not ApoE*3 Leiden Mice Fed an Atherogenic Diet

    Directory of Open Access Journals (Sweden)

    Nuala Murphy

    2005-01-01

    Full Text Available Dietary antioxidants are reported to suppress cellular expression of chemokines and adhesion molecules that recruit monocytes to the artery wall during atherosclerosis. In the present study we measured the effect of feeding apoE*3 Leiden mice or their non-transgenic (C57BL littermates with atherogenic diets either deficient in, or supplemented with, dietary antioxidants (vitamin E, vitamin C and β-carotene for 12 weeks, on serum levels of CC (JE/MCP-1 and CXC (KC chemokines and soluble adhesion molecules (sVCAM-1, sICAM-1 and atherosclerotic lesion size. ApoE*3 Leiden mice developed gross hypercholesterolaemia, and markedly accelerated (10–20 fold; P < 0.0001 atherogenesis, compared with non-transgenic animals. Antioxidant consumption reduced lesion area in non-transgenic, but not apoE*3 Leiden, mice. Serum sVCAM-1 and sICAM-1 levels were significantly (P < 0.0001 increased (sVCAM-1 up to 3.9 fold; sICAM-1 up to 2.4 fold by 4—8 weeks in all groups, and then declined. The initial increase in the concentration of adhesion molecules was reduced by 38%— 61% (P < 0.05 by antioxidant consumption, particularly in non-transgenic mice. By contrast, serum chemokine levels tended to increase more rapidly from baseline in apoE*3 Leiden mice, compared with non-transgenic animals, but were unaffected by dietary antioxidants. We conclude that dietary antioxidants reduce circulating soluble adhesion molecules and atherosclerosis in C57BL mice.

  5. Interactions between rs5498 polymorphism in the ICAM1 gene and traditional risk factors influence susceptibility to coronary artery disease.

    Science.gov (United States)

    Sarecka-Hujar, Beata; Zak, Iwona; Krauze, Jolanta

    2009-06-01

    Coronary artery disease (CAD) depends on multiple genetic and environmental factors. Adhesion molecules are markers of endothelium dysfunction. Intercellular adhesion molecule-1 (ICAM-1) interacts with leukocyte integrins and promotes atherosclerotic process at the surface of endothelial cells. The aim of the study was to assess the association between ICAM1 rs5498 polymorphism and CAD and to establish whether there are any interactions between this polymorphism and traditional risk factors in determining the risk of CAD. We studied 191 cases with angiographically documented CAD and 203 controls with no signs of cardiovascular diseases. The ICAM1 polymorphism was genotyped using PCR-RFLP method. Data were analyzed with the STATISTICA 7.1 and EpiInfo 6 softwares. We did not observe significant differences in the distribution of genotypes and alleles of rs5498 between cases and controls. We only found a tendency to a higher prevalence of G allele carriers (AG + GG) in patients compared to controls (68 vs. 64%, P = 0.399). A synergistic effect of G allele carrier-state and smoking that had influenced the risk of CAD [synergy index multiplicative (SIM = 2.09)] was observed. Smoking carriers of G allele compared to non-smoking AA were more prevalent in CAD group (39.8%) than among controls (13.3%, P < 0.0001, OR 4.81). Moreover, there was also a synergistic effect between G allele carrier-state and an elevated level of triacylglycerols (TG) (SIM = 1.28) increasing the risk of CAD. There is a synergistic interaction between rs5498 genotype and smoking that increases the risk of CAD. PMID:19048183

  6. Up-regulation of ICAM-1mRNA and IL-1βmRNA in lung tissues of a rat model of COPD.

    Science.gov (United States)

    Ji, Mingli; Wang, Yuxia; Li, Xiaopeng; Qian, Zhibin

    2015-01-01

    Chronic obstructive pulmonary disease (COPD) is a common respiratory disease characterized by airflow obstruction that is usually progressive and not fully reversible. It is accompanied by the abnormal inflammatory response of lung to toxic particles or gas. Studies indicate that chronic inflammatory injuries of airway, pulmonary parenchyma and pulmonary vessels are the characteristic changes of COPD. Adhesion of inflammatory cells is the important link of pulmonary infection. Intercellular adhesion molecule-1 (ICAM-1) is a glycoprotein involved in binding with mediated cells or with the extracellular matrix in the process called cell adhesion. IL-1β is an important inflammatory mediator as well as the promoter and critical inducer of cytokine cascade reaction. In this study, the rat model of COPD was established by smoking + intratracheal instillation of LPS (the experimental group). PaO2 and PaCO2 were measured. ICAM-1mRNA and IL-1βmRNA level in lung homogenate were detected by immunohistochemistry and RT-PCR and were compared with those of the rats treated by smoke exposure (the control group) and the healthy rats (the blank group) in order to investigate the effect of ICAM-1 and IL-1β in lung injury of COPD. This study showed that the respiratory function of rats with COPD was decreased. PaO2 of rats in the experimental group, the control group and the blank group decreased successively, and the comparison between any two groups had significant difference. PaCO2 increased successively, and the comparison between any two groups had significant difference. Immunohistochemistry results showed that protein expression of ICAM-1 and IL-1β in lung tissues of rats in the experimental group was higher than that in the control group and the blank group, and the comparison between any two groups had significant difference. RT-PCR results showed that ICAM-1mRNA and IL-1βmRNA level of rats in the experimental group was higher than that in the control group and the

  7. EXPRESSION OF ICAM-1 AND LFA-1 MOLECULES IN RELATION TO RENAL ALLOGRAFT REJECTION IN RATSA

    Institute of Scientific and Technical Information of China (English)

    黄孝伦; 沈文律; 李幼平; 周泽清; 谭建三

    1999-01-01

    Objective. The purpose of this study was to assess the renal graft expression of ICAM-I (intercellular adhesion moleculeq) and LFA l(lymphocyte function-aa.soziated antigen-1)molecule with relation to graft rejection. Methods. Rat kidney traansplantation was performed according to the procedure of Kamada with some modification. Experimental rats were dividod into 5 groups. The survival time of recipient rats and function of grafts after renal transplantation were observed. The sections of renal graft were mined forantibody ICAM-1 and LFA-1, and then quantification of ICAM-1 and LFA-1 expression was accomplished by computer image analysis. Results. ICAM-1 and LFA-1 increased significantly in the renal allograft rejection group as compared with the non-rejection groups(P<0. 05). Conclustion. Both biopsy of renal graft and monitoring of ICAM-1 and LFA-1 are useful tools in diagnosing and treating acute rejection.

  8. Expression of intercellular adhesion molecule-1 in rat heart with ischemia/reperfusion and limitation of infarct size by treatment with antibodies against cell adhesion molecules.

    OpenAIRE

    Yamazaki, T; Seko, Y; Tamatani, T; Miyasaka, M.; Yagita, H; Okumura, K.; R. Nagai; Yazaki, Y

    1993-01-01

    To elucidate the mechanism(s) of myocardial reperfusion injury, we investigated the roles of cell adhesion molecules on both leukocytes and vascular endothelial cells in the reperfused myocardia. We found that within 2 hours after reperfusion leukocytes began to infiltrate into the rat myocardia subjected to 30 minutes of ischemia and clarified, for the first time, that the expression of intercellular adhesion molecule-1 was enhanced on the capillary and venous endothelial cells from 8 to 96 ...

  9. Cell adhesion molecules involved in the leukocyte recruitment induced by venom of the snake Bothrops jararaca

    OpenAIRE

    Catarina F. P. Teixeira; Stella R. Zamuner

    2002-01-01

    It has been shown that Bothrops jararaca venom (BjV) induces a significant leukocyte accumulation, mainly neutrophils, at the local of tissue damage. Therefore, the role of the adhesion molecules intercellular adhesion molecule-1 (ICAM-1), LECAM-1, CD18, leukocyte function-associated antigen-1 (LFA-1) and platelet endothelial cell adhesion molecule-1 (PECAM-1) on the BjV-induced neutrophil accumulation and the correlation with release of LTB4, TXA2, tumor necrosis factor-alpha, interleukin (I...

  10. Intercellular adhesion molecule-1 expression in the hippocampal CA1 region of hyperlipidemic rats with chronic cerebral ischemia

    Institute of Scientific and Technical Information of China (English)

    Yingying Cheng; Ying Zhang; Hongmei Song; Jiachun Feng

    2012-01-01

    Chronic cerebral ischemia is a pathological process in many cerebrovascular diseases and it is induced by long-term hyperlipidemia, hypertension and diabetes mellitus. After being fed a high-fat diet for 4 weeks, rats were subjected to permanent occlusion of bilateral common carotid arteries to establish rat models of chronic cerebral ischemia with hyperlipidemia. Intercellular adhesion molecule-1 expression in rat hippocampal CA1 region was determined to better understand the mechanism underlying the effects of hyperlipidemia on chronic cerebral ischemia. Water maze test results showed that the cognitive function of rats with hyperlipidemia or chronic cerebral ischemia, particularly in rats with hyperlipidemia combined with chronic cerebral ischemia, gradually decreased between 1 and 4 months after occlusion of the bilateral common carotid arteries. This correlated with pathological changes in the hippocampal CA1 region as detected by hematoxylin-eosin staining. Immunohistochemical staining showed that intercellular adhesion molecule-1 expression in the hippocampal CA1 region was noticeably increased in rats with hyperlipidemia or chronic cerebral ischemia, in particular in rats with hyperlipidemia combined with chronic cerebral ischemia. These findings suggest that hyperlipidemia aggravates chronic cerebral ischemia-induced neurological damage and cognitive impairment in the rat hippocampal CA1 region, which may be mediated, at least in part, by up-regulated expression of intercellular adhesion molecule-1.

  11. Largazole, a class I histone deacetylase inhibitor, enhances TNF-α-induced ICAM-1 and VCAM-1 expression in rheumatoid arthritis synovial fibroblasts

    Energy Technology Data Exchange (ETDEWEB)

    Ahmed, Salahuddin, E-mail: Salah.Ahmed@utoledo.edu [Department of Pharmacology, College of Pharmacy and Pharmaceutical Sciences, The University of Toledo, OH (United States); Riegsecker, Sharayah; Beamer, Maria; Rahman, Ayesha; Bellini, Joseph V. [Department of Pharmacology, College of Pharmacy and Pharmaceutical Sciences, The University of Toledo, OH (United States); Bhansali, Pravin; Tillekeratne, L.M. Viranga [Department of Medicinal and Biological Chemistry, College of Pharmacy and Pharmaceutical Sciences, The University of Toledo, OH (United States)

    2013-07-15

    In the present study, we evaluated the effect of largazole (LAR), a marine-derived class I HDAC inhibitor, on tumor necrosis factor-α (TNF-α)-induced expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), and matrix metalloproteinase-2 (MMP-2) activity. LAR (1–5 μM) had no adverse effect on the viability of RA synovial fibroblasts. Among the different class I HDACs screened, LAR (0.5–5 μM) inhibited the constitutive expression of HDAC1 (0–30%). Surprisingly, LAR increased class II HDAC [HDAC6] by ∼ 220% with a concomitant decrease in HDAC5 [30–58%] expression in RA synovial fibroblasts. SAHA (5 μM), a pan-HDAC inhibitor, also induced HDAC6 expression in RA synovial fibroblasts. Pretreatment of RA synovial fibroblasts with LAR further enhanced TNF-α-induced ICAM-1 and VCAM-1 expression. However, LAR inhibited TNF-α-induced MMP-2 activity in RA synovial fibroblasts by 35% when compared to the TNF-α-treated group. Further, the addition of HDAC6 specific inhibitor Tubastatin A with LAR suppressed TNF-α + LAR-induced ICAM-1 and VCAM-1 expression and completely blocked MMP-2 activity, suggesting a role of HDAC6 in LAR-induced ICAM-1 and VCAM-1 expression. LAR also enhanced TNF-α-induced phospho-p38 and phospho-AKT expression, but inhibited the expression of phospho-JNK and nuclear translocation of NF-κBp65 in RA synovial fibroblasts. These results suggest that LAR activates p38 and Akt pathways and influences class II HDACs, in particular HDAC6, to enhance some of the detrimental effects of TNF-α in RA synovial fibroblasts. Understanding the exact role of different HDAC isoenzymes in RA pathogenesis is extremely important in order to develop highly effective HDAC inhibitors for the treatment of RA. - Highlights: • Largazole enhances TNF-α-induced ICAM-1 and VCAM-1. • Largazole upregulates class II HDAC (HDAC6) in RA synovial fibroblasts. • Largazole also induces the expression of phospho-p38

  12. 阿托伐他汀对高血压病患者血浆sICAM-1水平和PAI-1活性的影响%Effects of Atorvastatin on Plasma Level of sICAM-1 and PAI-1 Activity in Patients with Essential Hypertension

    Institute of Scientific and Technical Information of China (English)

    陈然; 黄红光; 刘江陵; 程春; 黄玉艳

    2011-01-01

    [Objective]To explore the change of plasma level of soluble intercellular adhesion molecule -1 (sICAM- 1) and plasminogen activator inhibitor-1(PAI-1) activity and the effect of atorvastatin on them in patients with essential hypertension.[Methods]Enzyme linked immunosorbent assay(ELISA) and spectrophotmetric assay were used to measure the plasma level of sICAM-1 and PAI-1 activity in 155 patients with mild to moderate essential hypertension before and after atorvastatin treatment and 8 normal controls.[Results]Plasma level of sICAM-1 and PAI-1 activity in hypertensive patients were significantly higher than those in normal controls( P <0.01 and P <0.05).Plasma level of sICAM-1 and PAI-1 activity in hypertensive patients significantly decreased after 8 weeks of atorvastatin treatment( P <0.01 and P <0.05).[Conclusion]Compared with normal people, the plasma level of sICAM-1 and PAI-1 activity in hypertensive patients increase significantly.Atorvastatin can not only decrease blood lipids, but also decrease the level of sICAM-1 and PAI-1 activity, and reduce the incidence of the complications of hypertension.%[目的]探讨高血压病(EH)患者血浆细胞间粘附分子-1(sICAM-1)水平和纤溶酶原激活物抑制剂-1(PAI-1)活性的变化及阿托伐他汀对其的影响.[方法]采用酶联免疫吸附法(ELISA)、发色底物显色法分别对155例轻至中度高血压患者应用阿托伐他汀治疗前后和正常对照组者血浆sICAM-1水平和PAI-1活性进行检测.[结果]高血压患者血浆sICAM-1水平和PAI-1活性明显高于正常对照组(P<0.01及P<0.05),经阿托伐他汀治疗8周后其浓度明显下降(P<0.01及P<0.05).[结论]高血压病患者血浆sICAM-1水平和PAI-1活性较正常人明显升高,阿托伐他汀在有效调脂的同时能降低高血压患者血sICAM-1浓度和PAI-1活性,减少高血压并发症的发生.

  13. KE and EE Genotypes of ICAM-1 Gene K469E Polymorphism Is Associated with Severe Preeclampsia

    Directory of Open Access Journals (Sweden)

    Ehsan Tabatabai

    2014-01-01

    Full Text Available Background. Preeclampsia (PE is one of the most important complications of pregnancy that is associated with significant mortality and morbidity in mother and fetus. Since the etiologic factors in its development are still unclear, we aimed to examine the intercellular adhesion molecule-1 (ICAM-1 gene K469E polymorphism in preeclamptic and control healthy women. Materials and Methods. Genetic polymorphism was analyzed in 192 PE and 186 healthy control women. PCR-RFLP method was used to identify K469E polymorphism. Results. The frequency of KK, KE, and EE genotypes of ICAM-1 gene was not different between PE patients and healthy pregnant women. Whereas, the frequency of KE and EE genotypes was significantly higher in severe PE than mild PE women and control group, and the risk of severe PE was 2.4-fold higher in subjects with KE genotype (OR, 2.4 [95% CI, 1 to 5.9]; P=0.03 and 3.3-fold higher in subjects with EE genotype (OR, 3.3 [95% CI, 1.2 to 9]; P=0.015 compared to individuals with KK genotype. Conclusion. We concluded that KE and EE genotypes of K469E polymorphism could increase risk of severe PE.

  14. Human rhinovirus 14 enters rhabdomyosarcoma cells expressing icam-1 by a clathrin-, caveolin-, and flotillin-independent pathway.

    Science.gov (United States)

    Khan, Abdul Ghafoor; Pickl-Herk, Angela; Gajdzik, Leszek; Marlovits, Thomas C; Fuchs, Renate; Blaas, Dieter

    2010-04-01

    Intercellular adhesion molecule 1 (ICAM-1) mediates binding and entry of major group human rhinoviruses (HRVs). Whereas the entry pathway of minor group HRVs has been studied in detail and is comparatively well understood, the pathway taken by major group HRVs is largely unknown. Use of immunofluorescence microscopy, colocalization with specific endocytic markers, dominant negative mutants, and pharmacological inhibitors allowed us to demonstrate that the major group virus HRV14 enters rhabdomyosarcoma cells transfected to express human ICAM-1 in a clathrin-, caveolin-, and flotillin-independent manner. Electron microscopy revealed that many virions accumulated in long tubular structures, easily distinguishable from clathrin-coated pits and caveolae. Virus entry was strongly sensitive to the Na(+)/H(+) ion exchange inhibitor amiloride and moderately sensitive to cytochalasin D. Thus, cellular uptake of HRV14 occurs via a pathway exhibiting some, but not all, characteristics of macropinocytosis and is similar to that recently described for adenovirus 3 entry via alpha(v) integrin/CD46 in HeLa cells.

  15. Human Rhinovirus 14 Enters Rhabdomyosarcoma Cells Expressing ICAM-1 by a Clathrin-, Caveolin-, and Flotillin-Independent Pathway ▿

    Science.gov (United States)

    Khan, Abdul Ghafoor; Pickl-Herk, Angela; Gajdzik, Leszek; Marlovits, Thomas C.; Fuchs, Renate; Blaas, Dieter

    2010-01-01

    Intercellular adhesion molecule 1 (ICAM-1) mediates binding and entry of major group human rhinoviruses (HRVs). Whereas the entry pathway of minor group HRVs has been studied in detail and is comparatively well understood, the pathway taken by major group HRVs is largely unknown. Use of immunofluorescence microscopy, colocalization with specific endocytic markers, dominant negative mutants, and pharmacological inhibitors allowed us to demonstrate that the major group virus HRV14 enters rhabdomyosarcoma cells transfected to express human ICAM-1 in a clathrin-, caveolin-, and flotillin-independent manner. Electron microscopy revealed that many virions accumulated in long tubular structures, easily distinguishable from clathrin-coated pits and caveolae. Virus entry was strongly sensitive to the Na+/H+ ion exchange inhibitor amiloride and moderately sensitive to cytochalasin D. Thus, cellular uptake of HRV14 occurs via a pathway exhibiting some, but not all, characteristics of macropinocytosis and is similar to that recently described for adenovirus 3 entry via αv integrin/CD46 in HeLa cells. PMID:20130060

  16. Evaluation of Liver Ischemia-Reperfusion Injury in Rabbits Using a Nanoscale Ultrasound Contrast Agent Targeting ICAM-1.

    Directory of Open Access Journals (Sweden)

    Fang Xie

    Full Text Available To assess the feasibility of ultrasound molecular imaging in the early diagnosis of liver ischemia-reperfusion injury (IRI using a nanoscale contrast agent targeting anti-intracellular adhesion molecule-1 (anti-ICAM-1.The targeted nanobubbles containing anti-ICAM-1 antibody were prepared using the avidin-biotin binding method. Human hepatic sinusoidal endothelial cells (HHSECs were cultured at the circumstances of hypoxia/reoxygenation (H/R and low temperature. The rabbit liver IRI model (I/R group was established using the Pringle's maneuver. The time-intensity curve of the liver contrast ultrasonographic images was plotted and the peak intensity, time to peak, and time of duration were calculated.The size of the targeted nanobubbles were 148.15 ± 39.75 nm and the concentration was 3.6-7.4 × 109/ml, and bound well with the H/R HHSECs. Animal contrast enhanced ultrasound images showed that the peak intensity and time of duration of the targeted nanobubbles were significantly higher than that of common nanobubbles in the I/R group, and the peak intensity and time of duration of the targeted nanobubbles in the I/R group were also significantly higher than that in the SO group.The targeted nanobubbles have small particle size, stable characteristic, and good targeting ability, which can assess hepatic ischemia-reperfusion injury specifically, noninvasively, and quantitatively at the molecular level.

  17. Upregulation of ICAM-1 Expression on J774.2 Macrophages by Endotoxin Involves Activation of NF-κB but not Protein Tyrosine Kinase: Comparison to Induction of iNOS

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    Hartmut Ruetten

    1999-01-01

    Full Text Available This study compares the signal transduction pathway which leads to the upregulation of intercellular adhesion molecule-1 (ICAM-1 expression with that of the increase in the expression of inducible nitric oxide synthase (iNOS protein and activity caused by endotoxin in cultured J774.2 macrophages. Treatment of J774.2 cells with lipopolysaccharide E. coli (LPS induced a concentration-dependent increase in the expression of ICAM-1 on the cell surface within 4 h and an increase in iNOS protein and activity at 24 h. The upregulation of ICAM-1 expression on J774.2 macrophages caused by LPS was significantly inhibited by pretreatment of the cells with inhibitors of the activation of the nuclear transcription factor NF-κB, such as L-1-tosylamido-2-phenylethylchloromethyl ketone (TPCK, pyrrolidine dithiocarbamate (PDTC, rotenone or calpain inhibitor I, but not by the tyrosine kinase inhibitors, tyrphostin AG126 or genistein. In contrast, genistein or tyrphostin AG126 also prevented the induction of iNOS protein and activity in J774.2 macrophages elicited by LPS. Thus, the increase in the expression of ICAM-1 on J774.2 macrophages by endotoxin involves the activation of NFκB, but not of protein tyrosine kinase.

  18. sICAM-1 intrathecal synthesis and release during the acute phase in children suffering from Coxsackie A9 and S. pneumoniae meningoencephalitis Sintesis intratecal de sICAM-1 y liberación durante la fase aguda en niños con meningoencefalitis por Coxsackie A9 y S pneumoniae

    Directory of Open Access Journals (Sweden)

    Alberto J. Dorta-Contreras

    2008-09-01

    Full Text Available The intercellular adhesion molecule is a transmembrane glycoprotein belonging to the immunoglobulin superfamily. Serum and cerebrospinal fluid (CSF soluble intercellular adhesion molecule 1 (sICAM-1 from normal control children as well as from children with Guillain-Barré syndrome (GBS, with Coxsackie A9 virus meningoencephalitis and with Streptococcus pneumoniae meningoencephalitis were studied. sICAM-1 was quantified using an immunoenzimatic assay and albumin using the immunodiffusion technique in both biological fluids. Increased sICAM-1 values in CSF in patients with GBS correspond to an increase of the albumin CSF/serum quotient. In contrast, in inflammatory diseases like S. pneumoniae and Coxsackie A9 virus meningoencephalitis an increased brain-derived fraction was observed. In particular cases these values are 60-65% and 70-75% respectively. The results indicate an additional synthesis of sICAM-1 in subarachnoidal space during central nervous system (CNS inflammatory process. An important role of sICAM-1 in the transmigration of different cell types into CSF during CNS inflammation in children with S. pneumoniae and Coxsackie A9 meningoencephalitis may be suggested.La molécula de adhesión intercelular es una glicoproteína que pertenece a la superfamilia de las inmunoglobulinas. Se estudiaron los niveles de molécula de adhesión intercelular tipo 1 soluble (sICAM-1 en suero y líquido cefalorraquídeo (LCR de niños con meningoencefalitis por Streptococcus pneumoniae y por Coxsackie A9 al igual que en niños con sindrome de Guillain-Barré (SGB. sICAM-1 fue cuantificado por ensayo inmunoenzimático y la albúmina por inmunodifusión en ambos líquidos biológicos. Los valores incrementados de sICAM-1 en LCR en los pacientes con GBS corresponden a valores aumentados de razón LCR/suero de albúmina. En contraste, en las enfermedades inflamatorias como las meningoencefalitis por S. pneumoniae y por Coxsackie A9 se observa un incremento

  19. Effects of alpha-lipoic acid on serum soluble intercellular adhesion molecule-1 and high sensitive-C reactive protein in patients with early diabetic nephropathy%α-硫辛酸对早期糖尿病肾病患者细胞间黏附分子-1和超敏C反应蛋白的影响

    Institute of Scientific and Technical Information of China (English)

    高云; 许娟

    2012-01-01

    Objective To investigate the effects of alpha-lipoic acid on serum soluble intercellular adhesion molecule-1 (sICAM-1) and high sensitive-C reactive protein (hs-CRP) levels in patients with early diabetic nephropathy (DN).Methods A total of 61 patients with early DN were randomized into treatment group (n =31 ) and control group ( n =30 ).The two groups were both treated with dietary control and oral hypoglycemic drugs or insulin.Meanwhile,the treatment group was additionally given alpha-lipoic acid 300 mg/d by intravenous infusion for 20 days.The levels of sICAM-1 and hs-CRP in each group were detected.Results The levels of sICAM-1 and hs-CRP were decreased significantly in alpha-lipoic acid treatment group after 20 days of therapy ( [ 198.03 ±23.67] μg/L vs [271.17 ±34.66] μg/L,[5.16 ±0.43] mg/Lvs [7.95 ±0.88]mg/L,P <0.01 ).Conclusion alpha-lipoic acid may decrease the expression of slCAM-1 and hs-CRP,and that may be one of the mechanisms to postpone the progress of early DN.%目的 探讨α-硫辛酸对早期糖尿病肾病(DN)患者可溶性细胞间黏附分子-1( sICAM-1)及超敏C反应蛋白(hs-CRP)的影响.方法 将61例早期DN患者分为治疗组31例及对照组30例,对照组常规饮食控制、口服降糖药或胰岛素处理,治疗组在此基础上加用α-硫辛酸300 mg加入到250 ml生理盐水中静脉滴注,1次/d,连续治疗20 d,测定两组患者的sICAM-1和hs-CRP浓度.结果 治疗组治疗后血清sICAM-1和hs-CRP较治疗前显著降低[(198.03±23.67)、(271.17±34.66) μg/L,(5.16±0.43)、(7.95±0.88) mg/L,t值分别为5.75、3.05,P均<0.01],差异均有统计学意义,对照组不显著.结论 早期DN患者接受α-硫辛酸治疗后sICAM-1和hs-CRP表达降低,提示α-硫辛酸抗氧化应激的同时,亦可能通过降低sICAM-1、hs-CRP的表达改善炎症状态而保护肾脏.

  20. Curcumin nanoparticles ameliorate ICAM-1 expression in TNF-α-treated lung epithelial cells through p47 (phox and MAPKs/AP-1 pathways.

    Directory of Open Access Journals (Sweden)

    Feng-Lin Yen

    Full Text Available Upregulation of intercellular adhesion molecule-1 (ICAM-1 involves adhesions between both circulating and resident leukocytes and the human lung epithelial cells during lung inflammatory reactions. We have previously demonstrated that curcumin-loaded polyvinylpyrrolidone nanoparticles (CURN improve the anti-inflammatory and anti-oxidative properties of curcumin in hepatocytes. In this study, we focused on the effects of CURN on the expression of ICAM-1 in TNF-α-treated lung epithelial cells and compared these to the effects of curcumin water preparation (CURH. TNF-αinduced ICAM-1 expression, ROS production, and cell-cell adhesion were significantly attenuated by the pretreatment with antioxidants (DPI, APO, or NAC and CURN, but not by CURH, as revealed by western blot analysis, RT-PCR, promoter assay, and ROS detection and adhesion assay. In addition, treatment of TNF-α-treated cells with CURN and antioxidants also resulted in an inhibition of activation of p47 (phox and phosphorylation of MAPKs, as compared to that using CURH. Our findings also suggest that phosphorylation of MAPKs may eventually lead to the activation of transcription factors. We also observed that the effects of TNF-α treatment for 30 min, which includes a significant increase in the binding activity of AP-1 and phosphorylation of c-jun and c-fos genes, were reduced by CURN treatment. In vivo studies have revealed that CURN improved the anti-inflammation activities of CURH in the lung epithelial cells of TNF-α-treated mice. Our results indicate that curcumin-loaded polyvinylpyrrolidone nanoparticles may potentially serve as an anti-inflammatory drug for the treatment of respiratory diseases.

  1. Concomitant upregulation of nuclear factor-kB activity, proinflammatory cytokines and ICAM-1 in the injured brain after cortical contusion trauma in a rat model

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    Hang Chun

    2005-01-01

    Full Text Available Background: Nuclear factor kappa B (NF-kB, proinflammatory cytokines and intercellular adhesion molecule 1 (ICAM-1 are frequently upregulated in the injured brain after traumatic brain injury (TBI. However, the temporal pattern of upregulation is not well defined. Aims: The current study was undertaken to investigate the temporal profile of the expression of NF-kB, proinflammatory cytokines and ICAM-1 in the injured brain after cortical contusion trauma of the rat brain. Settings and Design: A rat model of cortical contusion was produced by a free-falling weight on the exposed dura of right parietal lobe. The rats were randomly divided into control group and TBI groups at hours 3, 12, 24 and 72, and on day 7. Material and Methods: NF-kB binding activity in the surrounding brain of injured area was studied by electrophoretic mobility shift assay (EMSA. The levels of TNF-a and IL-6 were detected using ELISA and ICAM-1 expression studied by immunohistochemistry. Statistical analysis: The data were analyzed by one-way ANOVA followed by Student-Newman-Keuls post hoc test. Relation between variables was analyzed using bivariate correlation with two-tailed test. Results: Compared with that of control group, NF-kB binding activity in the injured brain was significantly increased through 12 h and 7 days postinjury, with the maximum at 72 h. The concentrations of TNF-a and IL-6 in the injured brain were significantly increased from 3 h to 7 days and maximal at 24 h postinjury. The number of ICAM-1 immunostained microvessels was significantly increased in the injured brain from 24 h to 7 days postinjury, with its peak at 72 h. Concomitant upregulation of TNF-a, IL-6, ICAM-1 and the cytokine mediators NF-kB in the injured brain was observed in the injured brain after cortical contusion, and there was a highly positive relation among these variables. Conclusions: Cortical contusion trauma could induce a concomitant and persistent upregulation of NF

  2. Silencing of PKC-α, TRPC1 or NF-κB expression attenuates cisplatin-induced ICAM-1 expression and endothelial dysfunction.

    Science.gov (United States)

    Bodiga, Vijaya Lakshmi; Kudle, Madhukar Rao; Bodiga, Sreedhar

    2015-11-01

    Platinum-based chemotherapy has been associated with increased long-term cardiovascular events. Also noteworthy is the accumulating awareness of early vascular toxicity occurring at the time of chemotherapy or immediately thereafter. The objective of the study was to delineate the molecular mechanisms associated with the early vascular toxicity and test the molecular silencing approach towards attenuating the endothelial dysfunction during platinum-based chemotherapy. Human umbilical vein endothelial cells (HUVECs) were treated with varying concentrations of cisplatin (1.0-10.0μg/ml) or vehicle control (0.1% dimethyl sulfoxide) for monitoring the changes in Intercellular adhesion molecule-1 (ICAM-1) mRNA and protein expression viz. a viz. altered activation of protein kinase C (PKC) isoforms, transient receptor potential channel (TRPC) 1 expression, Nuclear factor 'kappa-light-chain-enhancer' of activated B-cells (NF-κB), Store Operated Ca(2+) Entry (SOCE) in cisplatin-induced endothelial permeability and adherence of the activated endothelial cells to human monocyte-like U937 cells. Silencing of either PKC-α, TRPC1 or p65 subunit of NF-κB, all resulted in significant alleviation of cisplatin-induced endothelial dysfunction. At concentrations ≥8μg/ml, cisplatin induced a significant increase in the expression of ICAM-1 mRNA as well as protein. This was mediated by changes in PKC-α membrane translocation, NF-κB activation, increased expression as well as phosphorylation of TRPC1 and enhanced SOCE, leading to hyperpermeability and leakage of albumin. Increased adherence of U937 monocytes to cisplatin-activated endothelial cells was evident. Cisplatin challenge activates PKC-α, which in turn phosphorylated TRPC1 resulting in enhanced Ca(2+) entry. Increased Ca(2+) flux is required for activation of NF-κB and ICAM-1 expression. Enhanced ICAM-1 expression promotes monocyte binding to endothelial cells and increased endothelial hyperpermeability. PMID:26300057

  3. THE EFFECTS OF NF-KB ON ICAM-1 PROTEIN EXPRESSIONS OF RAT DURA MATER WITH MIGRAINE%NF-κB上调偏头痛大鼠脑膜ICAM-1蛋白表达

    Institute of Scientific and Technical Information of China (English)

    何秋; 王怀良; 章新华; 陈磊

    2007-01-01

    目的:探讨核转录因子-κB(nuclear factor-kappa B,NF-κB)在偏头痛脑膜炎症反应中的作用及细胞间黏附分子-1(intercellular adhesion molecules-1,ICAM-1)表达的调控机制.方法采用静脉注射(iv)硝酸甘油(glyceryl trinitrate,GTN)法建立大鼠偏头痛模型,分为对照组、模型组、溶剂对照组、吡咯烷二硫氨基甲酸(pyrrolidine dithiocarbamate,PDTC)组.各组分别包括0.9%生理盐水或GTN iv后1.5,4h两个实验小组.应用Western印迹法分别观察PDTC对GTN iv后1.5h大鼠脑膜NF-κB蛋白表达水平与GTN iv后4h ICAM-1蛋白表达水平的影响.结果:PDTC 50,100,200 mg.kg-1各剂量组GTN iv后1.5h大鼠脑膜NF-κB蛋白表达量较模型组分别降低30%(P<0.05)、52%(P<0.01)和65%(P<0.01),呈剂量依赖性;PDTC 50,100,200 mg.kg-1各剂量组GTN iv后4h大鼠脑膜ICAM-1蛋白表达量较模型组分别降低36%(P<0.05)、71%(P<0.01)和51%(P<0.01),无剂量依赖关系.结论:NF-κB参与偏头痛时脑膜ICAM-1的蛋白合成调控,在偏头痛的脑膜炎症机制中起着重要作用.

  4. 不同吸烟量对大鼠气道上皮细胞中细胞问黏附分子1表达的影响%Effects of different smoking quantity on expressions of intercellular adhesion molecule-1 in rat airway endothelial cells

    Institute of Scientific and Technical Information of China (English)

    索耀君; 许建英

    2009-01-01

    Objective To study the relationship between smoking as well as smoke abatement and airway inflammation of chronic obstructive pulmonary disease (COPD) through researching effects of different smoking quantity and different smoking time,smoking and smoke abatement on expression of intercellular adhesion molecule-1 (ICAM-1) in airway endothelial cells in rat model of smoking.Methods Forty Wistar rats were randomly divided into control group,long-term multiplicity smoking group,long-term manipulus smoking group,short-term multiplicity smoking group and smoke abatement group,eight rats in a group.The expressions of ICAM-1 in airway endothelial cells of rats were detected by immunohistochemistry and hybridization in situ.Results The expression of ICAM-1 mRNA and protein level in bronchial endothelial cells of long-term multiplicity smoking group were (6.93±1.44,19.22±0.22),short-term multiplicity smoking group (2.92±0.67,12.91±1.31 ),long-term manipulus smoking group (4.76±0.68, 14.03±2.39) and smoke abatement group (4.84±0.94,14.95±1.82),which were significantly increased compared with those of control group (1.45±0.98,8.83±0.77 ),peaking in the long-term multiplicity smoking group( P<0.05).The expression of ICAM-1 in bronchial endothelial cells of long-term manipulus smoking group,short-term multiplicity smoking group,smoke abatement group and the control group were lower than that of long-term multiplicity smoking group( P<0.05).Conclusions Smoking can result in the high expression of ICAM-1 mRNA and protein level in airway endothelial cells of rat model.The expression of ICAM-1 mRNA and protein level increase with the augmentation of smoking time and quantity and decrease after smoke abatement.It means smoke abatement can relieve airway inflammation but can not eliminate the change.Smoking abatement is an effective measure of preventing COPD.%目的 通过研究不同吸烟量、不同吸烟持续时间吸烟及戒烟对大鼠气道上皮

  5. Intercellular adhesion molecule-1 and gelatinase expression in human peritoneal mesothelial cells during propagation in culture.

    NARCIS (Netherlands)

    Sikkink, C.J.J.M.; Reijnen, M.M.P.J.; Duffhues, B.A.; Man, B.M. de; Lomme, R.M.L.M.; Goor, H. van

    2009-01-01

    Mesothelial cells are involved in a variety of biological processes, which include the formation of peritoneal adhesions. The cultures of human peritoneal mesothelial cells comprise an important tool to investigate the behavior and functions of mesothelial cells. Very little is known about the diffe

  6. Cytotoxicity, oxidative stress and expression of adhesion molecules in human umbilical vein endothelial cells exposed to dust from paints with or without nanoparticles

    DEFF Research Database (Denmark)

    Mikkelsen, Lone; Jensen, Keld A; Koponen, Ismo K;

    2013-01-01

    (VCAM-1) and intracellular adhesion molecule-1 (ICAM-1), but paint sanding dust samples generally generated less response than primary particles of TiO(2) and carbon black. We found no relationship between the expression of adhesion molecules, cytotoxicity and production of reactive oxygen species...

  7. Upregulation of endogenous ICAM-1 reduces ovarian cancer cell growth in the absence of immune cells

    NARCIS (Netherlands)

    de Groote, Marloes L.; Kazemier, Hinke G.; Huisman, Christian; van der Gun, Bernardina T. F.; Faas, Marijke M.; Rots, Marianne G.

    2014-01-01

    Ovarian cancer is a difficult-to-treat cancer with a 5-year survival rate of only approximate to 45%, due to late diagnosis and therapy resistance. In need of new therapeutic approaches, induction of intercellular adhesion molecule (ICAM)-1 expression might be of interest, since the expression of IC

  8. Effect of various metals on intercellular adhesion molecule-1 expression and tumour necrosis factor alpha production by normal human keratinocytes.

    Science.gov (United States)

    Guéniche, A; Viac, J; Lizard, G; Charveron, M; Schmitt, D

    1994-01-01

    Nickel, cobalt and chromium are metals very often implicated in allergic contact dermatitis. In vivo, keratinocytes, which are the first target cells, can be directly activated to participate in the local reaction, especially through the expression of the membrane antigen ICAM-1, a ligand of the leucocyte antigen LFA-1, and the production of cytokines. Our aim was to assess the effects of sensitizing metal haptens (nickel, cobalt and chromium) compared with the toxic metal cadmium on the induction of ICAM-1 and the production of TNF alpha by epidermal cells. For this purpose, normal human keratinocytes obtained during plastic skin surgery were cultured in low-calcium defined medium (MCDB153) and the metals were used in non-toxic concentrations. Using FACS analysis, ICAM-1 expression was found to be induced only by nickel. This stimulation appeared as early as 24 h after stimulation. All the metals induced a low expression of TNF alpha detectable by immunocytochemistry correlating with the induction of the nuclear stress protein Hsp72 which is closely linked genetically with the TNF alpha locus. However, only Ni2+, Co2+ and Cr2+ induced a significant release of TNF alpha detectable by ELISA after 48 h stimulation. This secretion was lower than that observed with known stimulants such as lipopolysaccharide. These results indicate that the metals studied are able to induce an aggressive cellular effect, and that nickel, by its ICAM-1 induction, may play a major role in the keratinocyte activation state during allergic contact dermatitis. PMID:7864660

  9. Apicobasal Polarity Controls Lymphocyte Adhesion to Hepatic Epithelial Cells

    Directory of Open Access Journals (Sweden)

    Natalia Reglero-Real

    2014-09-01

    Full Text Available Loss of apicobasal polarity is a hallmark of epithelial pathologies. Leukocyte infiltration and crosstalk with dysfunctional epithelial barriers are crucial for the inflammatory response. Here, we show that apicobasal architecture regulates the adhesion between hepatic epithelial cells and lymphocytes. Polarized hepatocytes and epithelium from bile ducts segregate the intercellular adhesion molecule 1 (ICAM-1 adhesion receptor onto their apical, microvilli-rich membranes, which are less accessible by circulating immune cells. Upon cell depolarization, hepatic ICAM-1 becomes exposed and increases lymphocyte binding. Polarized hepatic cells prevent ICAM-1 exposure to lymphocytes by redirecting basolateral ICAM-1 to apical domains. Loss of ICAM-1 polarity occurs in human inflammatory liver diseases and can be induced by the inflammatory cytokine tumor necrosis factor alpha (TNF-α. We propose that adhesion receptor polarization is a parenchymal immune checkpoint that allows functional epithelium to hamper leukocyte binding. This contributes to the haptotactic guidance of leukocytes toward neighboring damaged or chronically inflamed epithelial cells that expose their adhesion machinery.

  10. ICAM-1 expression and organization in human endothelial cells is sensitive to gravity

    Science.gov (United States)

    Zhang, Yu; Sang, Chen; Paulsen, Katrin; Arenz, Andrea; Zhao, Ziyan; Jia, Xiaoling; Ullrich, Oliver; Zhuang, Fengyuan

    2010-11-01

    Transendothelial migration (TEM) of immune cells is a crucial process during a multitude of physiological and pathological conditions such as development, defense against infections and wound healing. Migration within the body tissues and through endothelial barriers is strongly dependent and regulated both by cytoskeletal processes and by expression of surface adhesion molecules such as ICAM-1 and VCAM-1. Space flight experiments have confirmed that TEM will be inhibited and may cause astronauts' immune function decreased and make them easy for infection. We used NASA RCCS to provide a simulated microgravity environment; endothelial cells were cultured on microcarrier beads and activated by TNF-α. Results demonstrate after clinorotation ICAM-1 expression increased, consistent with the notion in parabolic flights. However, VCAM-1 showed no significant change between activated or inactivated cells. Depolymerization of F-actin and clustering of ICAM-1 on cell membrane were also observed in short-term simulated microgravity, and after 24 h clinorotation, actin fiber rearrangement was initiated and clustering of ICAM-1 became stable. ICAM-1 mRNA and VCAM-1 mRNA were up-regulated after 30 min clinorotation, and returned to the same level with controls after 24 h clinorotation.

  11. Influence of tongxinluo on microvascular intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 expression in rat brain ischemia-reperfusion model%通心络对大鼠脑缺血再灌注模型微血管细胞间黏附分子1和血管细胞黏附分子1表达的影响

    Institute of Scientific and Technical Information of China (English)

    赵忠新; 夏斌; 王春燕; 田国红

    2006-01-01

    property and suppressing platelet congregation capability, tongxinluo preparation has been proved by traditional Chinese medicine to possess certain function for protecting endothelial cells.OBJECTIVE: To observe the influence of Chinese medicinal herb "tongxinluo" compound on adhesion molecule expression in brain ischemia-reperfusion (IR) animal model.DESIGN: Randomized and controlled experiment.SETTING: Department of Neurology, Changzheng Hospital Affiliated to the Second Military Medical University of Chinese PLA.MATERIALS: This experiment was conducted at the laboratory of the Department of Neurology, Shanghai Changzheng Hospital, between October 2002 and January 2003. Totally 25 male SD rats were randomized into sham-operation group of 5 rats, model group of 10 rats and tongxinluo group of 10 rats.METHODS: Middle cerebral artery was occluded using thread-bolt method to induce focal brain IR model in rats. In sham-operation group,nylon thread was placed around the external carotid artery approximating to the branch of internal carotid artery, and the other procedure was the same as that in model group. Rats in tongxinluo group were given tongxininfusion before IR for 1 consecutive week, which was replaced by physiological saline of the same dosage in model group and sham-operation group. Brain tissues were obtained under anesthesia condition and cut into slices; conventional HE staining, immunohistochemical and in situ hybridization staining were conducted.MAIN OUTCOME MEASURES:① The number of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1)positive microvessels following IR injury.② The number of ICAM-1 and VCAM-1 mRNA positive microvessels following IR injury.RESULTS:① In sham-operation group,ICAM-1,VCAM-1 protein andICAM-1 mRNA positive microvessels could not be observed in hemispheric cortex and basal ganglion at the operative side.② In model group,the positive expression of ICAM-1, VCAM-1 protein and ICAM-1 m

  12. Intercellular Adhension Molecule-1 in the Pathogenesis of Heroin-induced Acute Lung Injury in Rats

    Institute of Scientific and Technical Information of China (English)

    周琼; 白明; 邹世清

    2004-01-01

    The expression of intercellular adhesion molecule-1 (ICAM-1) in the pathogenesis of heroin-induced acute lung injury (ALI) in rats was investigated. The model of ALI was established by intravenous injection of heroin into tail vein in rats. Thirty-six rats were randomly divided into heroin-treated groups (1 h, 2 h, 4 h, 6 h and 24 h) and normal control group. Changes in histopathologic morphology and biological markers of ALI were measured. The expression of ICAM-1in lung tissue was detected by using immunohistochemistry and RT-PCR. The results showed that the W/D ratio and protein contents in BALF of the heroin-treated groups were significantly higher than that of the control group (P<0.01). The histopathological changes in the lung tissue were more obvious in heroin-treated groups. The ICAM-1 protein and mRNA expression in the lung tissue of heroin-treated groups were significantly increased as compared with that of the control group (P<0.01), and correlated with the ALI parameters in a time-dependent manner. Increasing of ICAM-1 expression was involved in the formation of heroin-induced lung injury. Furthermore, the level of expression was positively correlated with the severity of lung injury.

  13. Interleukin 3 stimulates proliferation and triggers endothelial-leukocyte adhesion molecule 1 gene activation of human endothelial cells.

    Science.gov (United States)

    Brizzi, M F; Garbarino, G; Rossi, P R; Pagliardi, G L; Arduino, C; Avanzi, G C; Pegoraro, L

    1993-06-01

    Proliferation and functional activation of endothelial cells within a tissue site of inflammation are regulated by humoral factors released by cells, such as T lymphocytes and monocytes, infiltrating the perivascular space. In the present study we investigated the effects of interleukin 3 (IL-3), an activated T lymphocyte-derived cytokine, on cultured human umbilical vein endothelial cells (HUVEC). Proliferative activity, evaluated both by estimation of the fraction of cells in the S phase and by direct cell count demonstrated that IL-3, at the dose of 25 ng/ml, enhances more than threefold both DNA synthesis and cell proliferation above baseline control conditions. Binding studies with radioiodinated ligand demonstrated that HUVEC constitutively express a smaller number of IL-3 binding sites (approximately 99 binding sites per cell, with an apparent Kd of 149 pM). Accordingly, molecular analysis showed the presence of transcripts for both alpha and beta subunits of the IL-3 receptor. Functional activation of endothelial cells was evaluated by the expression of the endothelial-leukocyte adhesion molecule 1 (ELAM-1) transcript and by leukocyte adhesion. The ELAM-1 gene transcript was clearly detectable 4 h after IL-3 addition and started to decrease after 12 h. Moreover, IL-3-induced ELAM-1 transcription was followed by enhanced adhesion of neutrophils and CD4+ T cells to HUVEC. The findings that IL-3 can stimulate both proliferation and functional activation of endothelial cells suggest that this cytokine can be involved in sustaining the process of chronic inflammation.

  14. 电针丰隆穴对高脂血症大鼠腹腔巨噬细胞CD11b、ICAM-1表达的影响%Effect of Electroacupuncture at Point Fenglong on the Expressions of Peritoneal Macrophage CD11b and ICAM-1 in Hyperlipidemia Rats

    Institute of Scientific and Technical Information of China (English)

    王琼; 田佳玉; 肖颖; 张红星

    2014-01-01

    目的:观察电针丰隆穴对高脂血症大鼠巨噬细胞表面抗原CD11b、细胞间黏附分子-1(ICAM-1)表达的影响。方法将40只健康SD大鼠随机分为正常对照组、高脂饲料组、高脂+普通饲料组、高脂饲料治疗组及高脂+普通饲料治疗组。电针丰隆穴治疗28 d后,检测各组大鼠血脂水平,即总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)含量,流式细胞术(flow cytometry,FCM)检测各组大鼠腹腔巨噬细胞表面抗原CD11b、ICAM-1表达。结果高脂饲料组大鼠血浆TC、LDL-C较正常对照组明显上升(P<0.01);高脂+普通饲料组大鼠血清TC、LDL-C与高脂饲料组比较明显下降(P<0.01),较正常对照组仍升高明显(P<0.01);电针丰隆穴治疗后,大鼠血浆 TC、LDL-C 明显下降(P<0.01);TG、HDL-C变化不明显(P>0.05)。高脂饲料组大鼠巨噬细胞CD11b、ICAM-1表达率较正常对照组明显上升(P<0.01),高脂+普通饲料组大鼠巨噬细胞CD11b、ICAM-1表达率较高脂饲料组明显下降(P<0.05),较正常对照组仍明显上升(P<0.01),高脂饲料治疗组与高脂饲料组比较,CD11b、ICAM-1表达率明显下降(P<0.01),高脂+普通饲料治疗组与高脂+普通饲料组比较,CD11b、ICAM-1表达率明显降低(P<0.01),高脂+普通饲料治疗组与高脂饲料治疗组比较,CD11b、ICAM-1表达率明显降低(P<0.01)。相关分析显示,CD11b与ICAM-1水平呈显著正相关(r=0.947,P<0.01)。结论电针丰隆穴能够明显下调高脂血症大鼠血脂中TC、LDL-C水平,下调高脂血症大鼠巨噬细胞CD11b、ICAM-1的表达,对高脂血症具有一定的治疗作用。%Objective To investigate the effect of electroacupuncture at point Fenglong(ST40) on the expressions of macrophage surface antigen CD11b and intercellular adhesion molecule-1 (ICAM-1) in hyperlipidemia rats. Method Forty healthy SD rats were randomly allocated

  15. Pre-diagnostic levels of adiponectin and soluble vascular cell adhesion molecule-1 are associated with colorectal cancer risk

    Institute of Scientific and Technical Information of China (English)

    Mathilde Touvier; Pilar Galan; Sébastien Czernichow; Léopold Fezeu; Namanjeet Ahluwalia; Chantal Julia; Nathalie Charnaux; Angela Sutton; Caroline Méjean; Paule Latino-Martel; Serge Hercberg

    2012-01-01

    AIM:To examine the relationships between pre-diag-nostic biomarkers and colorectal cancer risk and assess their relevance in predictive models.METHODS:A nested case-control study was designed to include all first primary incident colorectal cancer cases diagnosed between inclusion in the SUpplementation en VItamines et Minéraux AntioXydants cohort in 1994 and the end of follow-up in 2007.Cases (n =50) were matched with two randomly selected controis (n =100).Conditional logistic regression models were used to investigate the associations between prediagnostic levels of hs-CRP,adiponectin,leptin,soluble vascular cell adhesion molecule-1 (sVCAM-1),soluble intercellular adhesion molecule-1,E-selectin,monocyte chemoattractant protein-1 and colorectal cancer risk.Area under the receiver operating curves (AUC) and relative integrated discrimination improvement (RIDI) statistics were used to assess the discriminatory poten tial of the models.RESULTS:Plasma adiponectin level was associated with decreased colorectal cancer risk (P for linear trend =0.03).Quartiles of sVCAM-1 were associated with increased colorectal cancer risk (P for linear trend =0.02).No association was observed with any of the other biomarkers.Compared to standard models with known risk factors,those including both adiponectin and sVCAM-1 had substantially improved performance for colorectal cancer risk prediction (P for AUC improvement =0.01,RIDI =26.5%).CONCLUSION:These results suggest that pre-diagnostic plasma adiponectin and sVCAM-1 levels are associated with decreased and increased colorectal cancer risk,respectively.These relationships must be confirmed in large validation studies.

  16. 不同冠心病血清soL-CXCL16,soL-ICAM1及hsCRP水平研究%The level and clinical significance of sol-CXCL16,sol-ICAM1and hsCRP in patients with different coronary heart diseases

    Institute of Scientific and Technical Information of China (English)

    陈阳

    2011-01-01

    目的 探讨不同冠心病血清soL-CXCL16,soL-ICAM1及hsCRP水平及临床意义.方法 选取冠心病患者61例,其中急性冠状动脉综合征(ACS)患者30例(ACS组),稳定型心绞痛(SAP)患者31例(SAP组),另选30例正常志愿者作为正常对照组.所有患者均检测soL-CXCL16,soL-ICAM1及hsCRP水平.并随访6个月的主要不良心血管病事件(MACE).结果 ACS组比SAP组有较高的soL-CXCL16(P<0.05),soL-ICAM1(P<0.01)及hsCRP(P<0.05)水平,且2组均显著性高于正常对照组(P<0.05或P<0.01).CXCL16与hsCRP、TG、CHO、LDL,存在相关性,而与其他指标均无相关性;但在ACS组、soL-CXCL16与soL-ICAM1有相关性,与其他指标无相关性.结论 检测soL-CXCL16、soL-ICAM1及hsCRP水平对冠心病有一定的临床诊断和预测意义.%Objective To explore the serum level and their clinical significance of high-sensitivity C- reactive protein(hs- CRP), soluble CXC chemokine iigand 16 (sol - CXCL16) and soluble vascular cell adhesion molecule - 1 ( sol - VCAM - 1 ) in patients with different coronary heart diseases(CHD). Methods Sixty one patients with CHD are randomized into acute coronary syndrome group(ACS group, 30 cases)and stable angina pectoris group(SAP group, 31 cases), and 30 volunteers are selected as controls. Serum levels of sol - CXCL16, sol - ICAM1 and hsCRP are measured by enzyme - linked immunosorbent assay. Results The Serum levels of sol - CXCL16( P< 0.05 ), sol - ICAM1 ( P < 0.01 ) and hsCRP ( P < 0.05) in ACS group are higher than that in SAP group, which in both groups are higher than that in control(P<0.05 or P<0.01). the level of sol - CXCL16 correlate with the levels of hsCRP, TG, CHO and LDL in all the selected ,while it correlate with the level of sol - ICAM1 only in ACS group. Conclusion To detect the Serum levels of sol - CXCL16, sol - ICAM1 and hsCRP has some clinical diagnosis and prognostic significance to coronary heart disease.

  17. 贝前列素钠对老年2型糖尿病合并下肢血管病变患者血清TNF-α、sICAM-1的影响%Beraprost sodium on patients with lower extremity vascular disease patients and serum in patients with type 2 diabetes Effects of TNF-α,sICAM-1

    Institute of Scientific and Technical Information of China (English)

    周波

    2014-01-01

    Objective To observe the serum tumor necrosis factor-beraprost sodium on elderly patients with type 2 diabetic patients with lower extremity vascular disease alpha (TNF-α),soluble intercellular adhesion molecule-1 (sI-CAM-1)effect.Methods 160 cases of elderly patients with type 2 diabetic patients with lower extremity vascular dis-ease,divided into the control group (80 cases)and observation group (80 cases).Two groups were treated with routine drugs to control blood sugar.Control group:Aspirin Enteric-coated Tablets 75mg,oral,qd.The observation group:beraprost sodium,oral administration of 40μg,tid.ELISA was used to detect serum TNF-α,sICAM-1 before and after treatment.Results The control group before and after treatment the serum TNF-α,sICAM-1 had no significant change (P>0.05);and the observation group after treatment,serum TNF-α,sICAM-1 were significantly lower than those be-fore therapy and control group after treatment (P<0.05)level.Conclusion beraprost sodium has a better therapeutic effect on vascular disease in the lower limbs in aged patients with type 2 diabetes mellitus,expression can significantly decrease the serum TNF-α,sICAM-1 .%目的:观察贝前列素钠对老年2型糖尿病合并下肢血管病变患者血清肿瘤坏死因子-α(TNF-α)、可溶性细胞间粘附分子-1(sICAM-1)的影响。方法选择老年2型糖尿病合并下肢血管病变患者160例,分为对照组(80例)和观察组(80例)。两组均给予常规药物控制血糖。对照组:阿司匹林肠溶片75 mg,口服,qd。观察组:贝前列素钠,40μg,口服,tid;6个月。采用 ELISA法检测用药前后血清 TNF-α、sICAM-1。结果对照组用药前后血清 TNF-α、sICAM-1无明显变化(P>0.05);而观察组用药后血清 TNF-α、sICAM-1均明显低于用药前及对照组用药后水平(P<0.05)。结论贝前列素钠能明显降低老年2型糖尿病合并下肢血管病变患者血清TNF-α、sICAM-1的表达。

  18. 经鼻持续气道正压通气对糖尿病肾病伴阻塞性睡眠呼吸暂停患者VEGF及ICAM-1的影响%Effects of Nasal Continuous Positive Airway Pressure on VEGF and ICAM - 1 of Diabetic Nephropathy Complicated with Obstructive Sleep Apnea Syndrome

    Institute of Scientific and Technical Information of China (English)

    邓刚; 姚丽君; 王小溶; 陈望燕

    2012-01-01

    Objective:To investigate the effects of nasal continuous positive airway pressure (nCPAP) on VEGF and ICAM - 1 of diabetic nephropathy (DN) complicated with obstructive sleep apnea syndrome (OSAS) patients. Methods :35 -62 years old subjects who presented as DN complicated with moderate to severe OSAS were recruited and divided into nCPAP treated group and control group. The plasma levels of blood glucose, cholesterol, glycosylated hemoglobin, creatinine and urinary protein excretion were measured by auto biochemistry analysis machine. The plasma levels of VEGF (vascular endothelial growth factor) and ICAM - 1 (intercellular Adhesion Molecule -1) were determined by ELISA. Results: After 3 months of nCPAP treatment, there was a significant decrease in circulating levels of VEGF and ICAM -1 as well as 24 hours urinary protein excretion in nCPAP treated group. Decreased urinary protein excretion rate presented a positive relationship to reduced plasma VEGF and ICAM - 1 levels separately. Conclusion: nCPAP treatment could reduce urinary protein excretion by decreasing plasma levels of VEGF and ICAM - 1 in DN complicated with OSAS patients.%目的:探讨经鼻持续气道正压通气( nasal continuous positive air pressure,nCPAP)治疗对糖尿病肾病(diabetic nephropathy,DN)伴阻塞性睡眠呼吸暂停综合征(obstructive sleep apnoea syndrome,OSAS)患者VEGF及ICAM -1的影响.方法:选择临床确诊的DN伴中度鼾症患者36例,年龄35岁~62岁.随机分为治疗组及对照组,对照组给予常规治疗血糖、血压以及血脂等药物,治疗组系在对照组基础上,同时给予nCPAP治疗3个月,检测指标:(1)血压、血糖、糖化血红蛋白、肾功能、血脂及24h尿蛋白定量等.(2)采用定量酶联免疫吸附试验(ELISA)检测血清VEGF、ICAM -1水平.(3)常规检测血氧饱和度(Sa02)及呼吸暂停低通气指数( apnea - hypopnea index,AHI).结果:经过3月的nCPAP治疗,两组治疗后患者血压、血肌酐、空腹血

  19. Expression and significance of ICAM-1 and its counter receptors LFA-1 and Mac-1 in experimental acute pancreatitis of rats

    Institute of Scientific and Technical Information of China (English)

    Wei Sun; Yasuhiro Watanabe; Zhong-Qiu Wang

    2006-01-01

    AIM: To investigate the role of intercellular adhesion molecule-1 (ICAM-1) and its counter receptors LFA-1 and Mac-1 in acute pancreatitis (AP).METHODS: SD rats were allocated to AP group and control group randomly (25 rats each). AP was induced by infusion of 5% chenodeoxycholic acid into the pancreatic duct, followed by ligation of pancreatic duct.The rats were sacrificed at 1, 3, 6, 12 and 24 h after induction of pancreatitis. Five rats were sacrificed at one time point in the two groups before the blood and specimens from pancreas and lung were obtained. Serum amylase and ascitic fluid were measured at each time point. Expression of ICAM-1 at different time points was assessed by immunohistochemistry in pancreas and lung,and the expression of LAF-1 and Mac-1 on neutrophils at different time points was detected by flow cytometer.RESULTS: Induction of AP was confirmed by the serum levels of amylase and histological studies. The expression of ICAM-1 in pancreas increased significantly than that in the control group at all time points (P<0.05 or P<0.01),as well as the expression in lung except at 1 h. The expression of LFA-1 and Mac-1 on neutrophil in blood increased significantly in AP group than that in control group at several time points (P<0.05 or P<0.01). The amount of ascitic fluid and serum amylase level of AP group increased significantly than that of control group at all time points (P<0.05 or P<0.01). Parallel to these results, a significant neutrophil infiltration was found in pancreas and lung tissues of AP group rats.CONCLUSION: Our findings suggest the important role for ICAM-1, LFA-1 and Mac-1 in mediating the development of AP from a local disease to a systemic illness. Upregulation of ICAM-1, LFA-1, Mac-1 and subsequent leukocyte infiltration appear to be significant events of pancreatic and pulmonary injuries in AP.

  20. Biodistribution and endocytosis of ICAM-1-targeting antibodies versus nanocarriers in the gastrointestinal tract in mice

    Directory of Open Access Journals (Sweden)

    Mane V

    2012-08-01

    Full Text Available Viraj Mane,1 Silvia Muro1, 21Institute for Bioscience and Biotechnology Research, 2Fischell Department of Bioengineering, University of Maryland, College Park, MD, USAAbstract: Drug delivery to the gastrointestinal (GI tract is key for improving treatment of GI maladies, developing oral vaccines, and facilitating drug transport into circulation. However, delivery of formulations to the GI tract is hindered by pH changes, degradative enzymes, mucus, and peristalsis, leading to poor GI retention. Targeting may prolong residence of therapeutics in the GI tract and enhance their interaction with this tissue, improving such aspects. We evaluated nanocarrier (NC and ligand-mediated targeting in the GI tract following gastric gavage in mice. We compared GI biodistribution, degradation, and endocytosis between control antibodies and antibodies targeting the cell surface determinant intercellular adhesion molecule 1 (ICAM-1, expressed on GI epithelium and other cell types. These antibodies were administered either as free entities or coated onto polymer NCs. Fluorescence and radioisotope tracing showed proximal accumulation, with preferential retention in the stomach, jejunum, and ileum; and minimal presence in the duodenum, cecum, and colon by 1 hour after administration. Upstream (gastric retention was enhanced in NC formulations, with decreased downstream (jejunal accumulation. Of the total dose delivered to the GI tract, ~60% was susceptible to enzymatic (but not pH-mediated degradation, verified both in vitro and in vivo. Attenuation of peristalsis by sedation increased upstream retention (stomach, duodenum, and jejunum. Conversely, alkaline NaHCO3, which enhances GI transit by decreasing mucosal viscosity, favored downstream (ileal passage. This suggests passive transit through the GI tract, governed by mucoadhesion and peristalsis. In contrast, both free anti-ICAM and anti-ICAM NCs demonstrated significantly enhanced upstream (stomach and duodenum

  1. U937泡沫细胞中细胞间粘附分子-1的表达及欧芹素乙的抑制作用%Expression of intercellular adhesion molecule-1 in U937 foam cells and inhibitory effect of imperatorin

    Institute of Scientific and Technical Information of China (English)

    杨鹏远; 芮耀诚; 李凯; 黄兴华; 蒋建明; 余龙

    2002-01-01

    目的:研究在人类单核细胞系U937泡沫细胞中,细胞间粘附分子-1(ICAM-1)的表达水平,观测欧芹素乙(欧前胡内酯,imperatorin,IMP)对ICAM-1表达的抑制作用.方法:将U937细胞与80mg/L氧化低密度脂蛋白孵育48h,建立U937泡沫细胞模型.在培养基中预加入不同浓度的IMP(0,25,50,100μmol/L).采用Western blotting检测ICAM-1的蛋白表达;采用Northern blotting检测ICAM-1的mRNA水平.结果:泡沫细胞中ICAM-1的表达显著高于正常U937细胞.ICAM-1的蛋白和mRNA水平分别是正常U937的15和10倍.经IMP50和100μmol/L预处理后,泡沫细胞中ICAM-1的高表达被显著抑制.当IMP浓度达到100 μmol/L时,ICAM-1的蛋白水平降低了79%,mRNA水平降低了74%.结论:经氧化低密度脂蛋白孵育后,U937泡沫细胞中ICAM-1呈现高表达,IMP能显著抑制这种表达.%AIM: To investigate the expression level of intercellularadhesion molecule-1 (ICAM-1) in a macrophage-derivedfoam cell model from human U937 cell line and theinhibitory effect of imperatorin (IMP) on the ICAM-1.METHODS: U937 cells were incubated with oxidizedlow density lipoprotein (ox-LDL) 80 mg/L for 48 h anda macrophage-derived foam cell model was established.The medium was pretreated with different concentrationsof IMP (0, 25, 50, 100 μmol/L). ICAM-1 proteinexpression in cells was measured with Western blotting;ICAM-1 mRNA level in cells was measured by Northernblotting. RESULTS: After incubated with ox-LDL,ICAM-1 expression level increased greatly. The increasein ICAM-1 protein level and mRNA level was estimatedto be about 15-fold and 10-fold. When the cells werepretreated with imperatorin (50, 100 μmol/L ), theincrease of ICAM-1 in foam cells were remarkablyinhibited. Especially when pretreated with IMP 100μmoL/L, the ICAM-1 protein level decreased by 79 %and the mRNA level decreased by 74 % each comparedto the level of foam cells. CONCLUSION: Afterincubated with ox-LDL in vitro, the U937 foam cellsshowed an

  2. Meta- analysis of association between K469E polymorphism of the ICAM-1 gene and retinopathy in type 2 diabetes

    Institute of Scientific and Technical Information of China (English)

    Wen-Ying; Fan; Ning-Pu; Liu

    2015-01-01

    AIM: To collectively evaluate the association of intercellular adhesion molecule-1(ICAM-1) gene K469 E polymorphism(rs5498) with diabetic retinopathy(DR) in patients with type 2 diabetic mellitus(T2DM). METHODS: Overall review of available literatures relating K469 E polymorphism to the risk of DR was conducted on 4 electronic databases. Meta-analysis was performed by Stata 12.0 to calculate pooled odds ratios(ORs). Potential sources of heterogeneity and bias were explored.RESULTS: Seven studies with genotype frequency data including 1120 cases with DR and 956 diabetic controls free of DR were included. Meta-analysis did not show significant association of K469 E polymorphism with DR(P >0.05). A statistically significant association was detected between the K469 E polymorphism and proliferative DR(PDR) in Asians only in dominant model(GG+AG vs AA) with pooled OR of 0.729(95%CI: 0.564-0.942, P=0.016, P heterogeneity=0.143), however, this association was not detected in recessive model(AG +AA vs GG;OR=1.178, 95%CI: 0.898-1.545, P =0.236, P heterogeneity=0.248)or allelic model(G vs A; OR=0.769, 95% CI: 0.576-1.026,P =0.074, P heterogeneity=0.094). No publication bias was found by Funnel plot, Begg’s and Egger’s test. CONCLUSION: This research found no statistically significant association between ICAM-1 gene K469 E polymorphism and DR in patients with T2 DM, but showed significant association of the K469 E polymorphism with PDR in Asian diabetic patients only in dominant model. Further investigation would be required to consolidate the conclusion.

  3. Effect of Fluvastatin on Oxidation-reduction Function and ICAM-1 Expression in Pocine Carotid Artery Endothelial Cells Dealt with Hypoxia/Reoxygenation

    Institute of Scientific and Technical Information of China (English)

    Fukuda Daiju; Sata Masataka; Toshiyuki Hagiwara; Kayoko Gomita

    2014-01-01

    Objective:To explore the protective function of lfuvastatinon endothelial cells in an ischemia-reperfusion process. Methods:Pocine carotid artery endothelial cells (PCAEC) were cultured, grown together with different concentrations of fluvastatin (0.1 μmol/L, 0.2 μmol/L, 0.5 μmol/L, 1.0 μmol/L) for 44 h, and then divided into normal control group, different concentrations of lfuvastatin groups and H/R group. Serum immunology and cell immunochemistry were used to detect the levels of methyl thiazolyl tetrazolium (MTT), glutathione peroxidase (GSH-PX), malondialdehyde (MDA), superoxide dismutase (SOD) and intercellular adhesion molecule-1 (ICAM-1) after 1-h hypoxia and 3-h reoxygenation. The effect of fluvastatin on oxidation-reduction function and ICAM-1 expression in PCAEC dealt with hypoxia/reoxygenation (H/R) was observed. Results:There was signiifcant difference regarding the cell viability between H/R group intervened by 0.5 μmol/L of lfuvastatin and simple H/R group (P=0.01). H/R could obviously decrease SOD activity in culture cells, and the generated MDA was conspicuously higher by comparison to lfuvastatin group and normal control group (P=0.001). Signiifcant differences were presented regarding GSH-PX level between normal control group, lfuvastatin group and H/R group (P=0.002). Additionally, ICAM-1 cell immunochemical staining showed marked differences among each group (P=0.018). Conclusion: Proper concentration of lfuvastatin can protect H/R endothelial cells.

  4. Dengue virus enhances thrombomodulin and ICAM-1 expression through the macrophage migration inhibitory factor induction of the MAPK and PI3K signaling pathways.

    Directory of Open Access Journals (Sweden)

    Trai-Ming Yeh

    Full Text Available Dengue virus (DV infections cause mild dengue fever (DF or severe life-threatening dengue hemorrhagic fever (DHF. The mechanisms that cause hemorrhage in DV infections remain poorly understood. Thrombomodulin (TM is a glycoprotein expressed on the surface of vascular endothelial cells that plays an important role in the thrombin-mediated activation of protein C. Prior studies have shown that the serum levels of soluble TM (sTM and macrophage migration inhibitory factor (MIF are significantly increased in DHF patients compared to levels in DF patients or normal controls. In this study, we investigated how MIF and sTM concentrations are enhanced in the plasma of DHF patients and the potential effect of MIF on coagulation through its influence on two factors: thrombomodulin (TM and intercellular adhesion molecule-1 (ICAM-1 in endothelial cells and monocytes. Recombinant human macrophage migration inhibitory factor (rMIF was used to treat monocytic THP-1 cells and endothelial HMEC-1 cells or primary HUVEC cells. The subsequent expression of TM and ICAM-1 was assessed by immunofluorescent staining and flow cytometry analysis. Additionally, the co-incubation of THP-1 cells with various cell signaling pathway inhibitors was used to determine the pathways through which MIF mediated its effect. The data provided evidence that severe DV infections induce MIF expression, which in turn stimulates monocytes or endothelial cells to express TM and ICAM-1 via the Erk, JNK MAPK and the PI3K signaling pathways, supporting the idea that MIF may play an important role as a regulator of coagulation.

  5. Effects of Estrogen Level on the Function of Vascular Endothelial Cells and Expression of Vascular Cell Adhesion Molecule - 1φ

    Institute of Scientific and Technical Information of China (English)

    WU Saizhu(吴赛珠); LIU Jiangguo(刘建国); TAN Jiayu(谭家余); ZHoU Kexiang(周可祥); Gorge D Webb; WEI Heming(隗和明); GUO Zhiguang(郭志刚)

    2002-01-01

    Objectives To ob- serve the effect of different estrogen levels on the se- cretory function of vascular endothelial cells of female rats, and study the effect of modulation of estrogen level on the expression of vascular cell adhesion molecule - 1 and the concentration of estrogen receptorin vascular endothelial cells. Methods Radioim-munology was used to measure the serum concentrationof endothelin and PGI2, and copper-cadmium re-duction was employed to measure the serum content ofnitrogen monoxide. Radioligand binding and flowcy-tometry were used to measure the expression of estrogenreceptor and vascular cell adhesion molecule (VCAM-1 ) of vascular endothelial cells respectively. Re-sults 1. The serum concentration of nitric oxide andPGI2 decreased when the ovaries of female rats wereremoved. In ovariectomized rats, given estrogen, theconcentration rose ( P < 0.05), but the plasma con-centration of endothelin was adverse to it. 2. Theconcentration of estrogen receptor of vascular endothe-lial cells decreased remarkably when the ovaries of fe-male rats were removed. When given estrogen, it in-creased. 3. The percent of expressed VCAM - 1 in-creased siguificantly after interleukin- lβoperated onthe cells, but 17 - βestradiol at 3 × 10-8 ~ 10-6 mol/lall decreased the percent. Conclusions Estrogenlevel can influence the secretion of nitrogen monoxide,PGI2 and endothlin of vascular endothelial cells, andalso influence the concentration of estrogen receptor ofvascular endothelial cells. 17 -β Estradiol at 3 × 10-8~ 10-6 M can decrease the elevation of VCAM - 1 ofvascular endothelial cells induced by interleukin - 1 β.

  6. Molecular MR Imaging for Visualizing ICAM-1 Expression in the Inflamed Synovium of Collagen-Induced Arthritic Mice

    Energy Technology Data Exchange (ETDEWEB)

    Lee, Sang Il [Gyeongsang National University, Jinju (Korea, Republic of); Lee, Sang Yong; Jang, Kyu Yun; Yoo, Wan Hee [Chonbuk National University, Jeonju (Korea, Republic of); Yoon, Kwon Ha [Wonkwang University School of Medicine, Iksan (Korea, Republic of); Choi, Kyu Sil [Sungkyunkwan University School of Medicine, Seoul (Korea, Republic of); Kim, Sang Hyon; Choi, Tae Hyun [Dongsan Medical Center, Keimyung University, Daegu (Korea, Republic of); Park, Jin Gyoon [Chonnam National University Medical School, Gwangju (Korea, Republic of)

    2009-10-15

    To determine the utility of intercellular adhesion molecule (ICAM)-1 antibody-conjugated gadolinium diethylenetriaminepentaacetic acid (Gd-DTPAanti- ICAM-1) as a targeted contrast agent for the molecular magnetic resonance imaging (MRI) in collagen-induced arthritis (CIA). Three groups of mice were used: non-arthritic normal, CIA mice in both the early inflammatory and chronic destructive phases. The MR images of knee joints were obtained before and after injection of Gd-DTPA-anti- ICAM-1, Gd-DTPA, and Gd-DTPA-Immunoglobulin G (Ig G) and were analyzed quantitatively. The patterns of enhancement on the MR images were compared with the histological and immunohistochemical ICAM-1 staining. The images obtained after injection of Gd-DTPA-anti-ICAM-1 displayed gradually increasing signal enhancement from the moment following injection (mean {+-} standard deviation [SD]: 424.3 {+-} 35.2, n = 3) to 24 hours (532 {+-} 11.3), rather than on pre-enhanced images (293 {+-} 37.6) in the early inflammatory phase of CIA mice. However, signal enhancement by Gd-DTPA and Gd- DTPA-IgG disappeared after 80 minutes and 24 hours, respectively. In addition, no significant enhancement was seen in the chronic destructive phase of CIA mice, even though they also showed inflammatory changes on T2-weighted MR images. ICAM-1 expression was demonstrated in the endothelium and proliferating synovium of the early inflammatory phase of CIA mice, but not in the chronic destructive phase. Molecular MRI with Gd-DTPA-anti-ICAM-1 displays specific images targeted to ICAM-1 that is expressed in the inflamed synovium of CIA. This novel tool may be useful for the early diagnosis and differentiation of the various stages of rheumatoid arthritis.

  7. The ICAM-1 469 T/C gene polymorphism but not 241 G/A is associated with Behcets disease in the Lebanese population

    International Nuclear Information System (INIS)

    To investigate the association of the 2 intracellular adhesion molecules-1 (ICAM-1) gene polymorphisms [thymidine/cytidine (T/C) 469 and guanosine/adenosine (G/A) 241] in Behcets disease in Lebanon. We initiated the study in July 2003, and carried out the work in the research laboratory of Beirut Arab University, Beirut, Lebanon. We extracted the DNA by glass fiber matrix mini column. We amplified the ICAM gene by polymerase chain reaction (PCR) and tested the PCR products for the presence of the polymorphisms using a restriction enzyme specific for each ----- +polymorphism. We analyzed the results by agarose electrophoresis. We demonstrated the association of only one single nucleotide polymorphism (SNP) (K469) with Behcets disease, while we could not detect the other SNP (G241A) in either controls or patients in the Lebanese population. The ICAM-1 gene polymorphism 469 T/C, but not 241 G/A, may encode risk for Behcets disease in the Lebanese population. (author)

  8. Artemether Combined with shRNA Interference of Vascular Cell Adhesion Molecule-1 Significantly Inhibited the Malignant Biological Behavior of Human Glioma Cells

    OpenAIRE

    Ying-Bin Wang; Yi Hu; Zhen Li; Ping Wang; Yi-Xue Xue; Yi-Long Yao; Bo Yu; Yun-Hui Liu

    2013-01-01

    Artemether is the derivative extracted from Chinese traditional herb and originally used for malaria. Artemether also has potential therapeutic effects against tumors. Vascular cell adhesion molecule-1 (VCAM-1) is an important cell surface adhesion molecule associated with malignancy of gliomas. In this work, we investigated the role and mechanism of artemether combined with shRNA interference of VCAM-1 (shRNA-VCAM-1) on the migration, invasion and apoptosis of glioma cells. U87 human glioma ...

  9. Study of serum soluble vascular cell adhesion molecule-1 levels in type 2 diabetic patients with diabetic retinopathy

    International Nuclear Information System (INIS)

    To study the change and the correlation of serum soluble vascular cell adhesion molecule-1 (sV-CAM-1) levels with diabetic retinopathy in type 2 diabetic patients, serum sVCAM-1 levels were measured in duplicate by ELISA in 85 type 2 diabetic patients; fundus examination was performed by an ophthalmologist using ophthalmoscope or fundus fluorescein angiography, and the findings were graded as: no signs of diabetic retinopathy (NDR), background diabetic retinopathy (BDR) and proliferative diabetic retinopathy (PDR). Serum sVCAM-1 levels were significantly higher in the PDR and BDR groups than those in the control and NDR groups respectively (P<0.01). NDR group showed significantly increased serum sVCAM-levels compared with control group (P<0.01). In contrast, serum sVCAM-1 levels were not related to the presence of blood glucose, serum insulin levels or known diabetic duration. Authors' results suggest that serum sVCAM-1 might be implicated in the development of the diabetic retinopathy, and could assess the severity of diabetic retinopathy. The measurement of serum sVCAM-1 levels in 2 type diabetic patients may be clinically useful for early diagnosis or treatment of diabetic retinopathy

  10. Milk IgA responses are augmented by antigen delivery to the mucosal addressin cellular adhesion molecule 1.

    Science.gov (United States)

    Johnson, Susan; Bourges, Dorothee; Wijburg, Odilia; Strugnell, Richard A; Lew, Andrew M

    2006-07-01

    The mucosal addressin cellular adhesion molecule 1 (MAdCAM) is expressed on the venules of the gut associated lymphoid tissue (GALT); it is also expressed on the venules of the lobules of the mammary gland. We have previously found that MAdCAM-targeting using a rat anti-MAdCAM monoclonal Ab as both antigen and targeting moiety resulted in an enhanced local IgA gut response. We therefore surmised that such targeting may also enhance IgA responses in the mammary gland. We show that our model antigen localizes to the lobules of the mammary glands as well as the GALT, but not to the draining lymph nodes and that targeting MAdCAM results in secretory IgA responses in the milk. We provide evidence that this milk IgA Ab is of a secretory nature and is consistent with derivation from gut plasmablasts that have migrated to the mammary gland. Targeting MAdCAM may be a way for a novel vaccine strategy that affords protection to the mammary gland and the suckling neonate. PMID:16723174

  11. Early Detection of Junctional Adhesion Molecule-1 (JAM-1 in the Circulation after Experimental and Clinical Polytrauma

    Directory of Open Access Journals (Sweden)

    Stephanie Denk

    2015-01-01

    Full Text Available Severe tissue trauma-induced systemic inflammation is often accompanied by evident or occult blood-organ barrier dysfunctions, frequently leading to multiple organ dysfunction. However, it is unknown whether specific barrier molecules are shed into the circulation early after trauma as potential indicators of an initial barrier dysfunction. The release of the barrier molecule junctional adhesion molecule-1 (JAM-1 was investigated in plasma of C57BL/6 mice 2 h after experimental mono- and polytrauma as well as in polytrauma patients (ISS ≥ 18 during a 10-day period. Correlation analyses were performed to indicate a linkage between JAM-1 plasma concentrations and organ failure. JAM-1 was systemically detected after experimental trauma in mice with blunt chest trauma as a driving force. Accordingly, JAM-1 was reduced in lung tissue after pulmonary contusion and JAM-1 plasma levels significantly correlated with increased protein levels in the bronchoalveolar lavage as a sign for alveolocapillary barrier dysfunction. Furthermore, JAM-1 was markedly released into the plasma of polytrauma patients as early as 4 h after the trauma insult and significantly correlated with severity of disease and organ dysfunction (APACHE II and SOFA score. The data support an early injury- and time-dependent appearance of the barrier molecule JAM-1 in the circulation indicative of a commencing trauma-induced barrier dysfunction.

  12. Neutrophils lacking platelet-endothelial cell adhesion molecule-1 exhibit loss of directionality and motility in CXCR2-mediated chemotaxis.

    Science.gov (United States)

    Wu, Yue; Stabach, Paul; Michaud, Michael; Madri, Joseph A

    2005-09-15

    Time-lapsed videomicroscopy was used to study the migration of platelet-endothelial cell adhesion molecule-1-deficient (PECAM-1(-/-)) murine neutrophils undergoing chemotaxis in Zigmond chambers containing IL-8, KC, or fMLP gradients. PECAM-1(-/-) neutrophils failed to translocate up the IL-8, KC, and fMLP gradients. Significant reductions in cell motility and cell spreading were also observed in IL-8 or KC gradients. In wild-type neutrophils, PECAM-1 and F-actin were colocalized at the leading fronts of polarized cells toward the gradient. In contrast, in PECAM-1(-/-) neutrophils, although F-actin also localized to the leading front of migrating cells, F-actin polymerization was unstable, and cycling was remarkably increased compared with that of wild-type neutrophils. This may be due to the decreased cytokine-induced mobilization of the actin-binding protein, moesin, into the cytoskeleton of PECAM-1(-/-) neutrophils. PECAM-1(-/-) neutrophils also exhibited intracellularly dislocalized Src homology 2 domain containing phosphatase 1 (SHP-1) and had less IL-8-induced SHP-1 phosphatase activity. These results suggest that PECAM-1 regulates neutrophil chemotaxis by modulating cell motility and directionality, in part through its effects on SHP-1 localization and activation. PMID:16148090

  13. Soluble Vascular Cell Adhesion Molecule-1 (VCAM-1) as a Biomarker in the Mouse Model of Experimental Autoimmune Myocarditis (EAM)

    Science.gov (United States)

    Grabmaier, U.; Kania, G.; Kreiner, J.; Grabmeier, J.; Uhl, A.; Huber, B. C.; Lackermair, K.; Herbach, N.; Todica, A.; Eriksson, U.; Weckbach, L. T.; Brunner, S.

    2016-01-01

    Vascular cell adhesion molecule-1 (VCAM-1) is strongly upregulated in hearts of mice with coxsackie virus-induced as well as in patients with viral infection-triggered dilated cardiomyopathy. Nevertheless, the role of its soluble form as a biomarker in inflammatory heart diseases remains unclear. Therefore, we investigated whether plasma levels of soluble VCAM-1 (sVCAM-1) directly correlated with disease activity and progression of cardiac dysfunction in the mouse model of experimental autoimmune myocarditis (EAM). EAM was induced by immunization of BALB/c mice with heart-specific myosin-alpha heavy chain peptide together with complete Freund`s adjuvant. ELISA revealed strong expression of cardiac VCAM-1 (cVCAM-1) throughout the course of EAM in immunized mice compared to control animals. Furthermore, sVCAM-1 was elevated in the plasma of immunized compared to control mice at acute and chronic stages of the disease. sVCAM-1 did not correlate with the degree of acute cardiac inflammation analyzed by histology or cardiac cytokine expression investigated by ELISA. Nevertheless, heart to body weight ratio correlated significantly with sVCAM-1 at chronic stages of EAM. Cardiac systolic dysfunction studied with positron emission tomography indicated a weak relationship with sVCAM-1 at the chronic stage of the disease. Our data provide evidence that plasma levels of sVCAM-1 are elevated throughout all stages of the disease but showed no strong correlation with the severity of EAM. PMID:27501319

  14. Increased concentrations of soluble vascular cell adhesion molecule-1 and soluble CD40L in subjects with metabolic syndrome.

    Science.gov (United States)

    Palomo, Iván G; Jaramillo, Julio C; Alarcón, Marcelo L; Gutiérrez, César L; Moore-Carrasco, Rodrigo; Segovia, Fabián M; Leiva, Elba M; Mujica, Verónica E; Icaza, Gloria; Dí, Nora S

    2009-01-01

    Metabolic syndrome (MS) is associated with a high incidence rate of cardiovascular disease. It is characterized by abdominal obesity, elevated blood pressure, atherogenic dyslipidemia [high LDL-c (low density lipoprotein cholesterol) and low HDL-c (high density lipoprotein cholesterol)] and insulin resistance or glucose intolerance. In the context of MS, alterations in the plasmatic levels of some soluble forms of cell adhesion molecules can appear, e.g., soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble E-selectin (sE-selectin) and soluble CD40L (sCD40L). The objective of this study was to compare the serum levels of sVCAM-1, sE-selectin and sCD40L in MS and non-MS groups and to associate these molecules with the diagnostic criteria of MS. A total of 185 non-smokers between 45 and 64 years of age were included. Of these, 93 corresponded to the MS group and the remaining 92 to a non-MS group (according to modified ATP III criteria). The serum concentration of sVCAM-1, sE-selectin and sCD40L was determined by commercial solid phase ELISA. The results were expressed as a median and interquartile range. The MS group showed high levels of sVCAM-1 (558.9 ng/ml; 481.3-667.6 ng/ml) compared with the non-MS group (405.2 ng/ml; 361.0-470.5 ng/ml) (p<0.0001). As well, the median level of sCD40L (3.0 ng/ml; 2.1l-11.7 ng/ml) was significantly higher in the MS group than that in the non-MS group (2.6 ng/ml; 2.3-3.4 ng/ml) (p=0.0061). sE-selectin levels did not differ significantly between the groups: 73.9 ng/ml (58.3-87.0 ng/ml) and 68.5 ng/ml (51.6-97.5 ng/ml) in the MS and non-MS group, respectively. In conclusion, the serum levels of sVCAM-1 and sCD40L, but not sE-selectin, were significantly higher in patients with MS than in subjects that did not present MS. MS may therefore increase the expression of cell adhesion molecules, probably through endothelial activation. PMID:21475854

  15. The neural cell adhesion molecule-derived peptide, FGL, attenuates lipopolysaccharide-induced changes in glia in a CD200-dependent manner

    DEFF Research Database (Denmark)

    Cox, F F; Berezin, V; Bock, E;

    2013-01-01

    200-deficient mice and preincubated with FGL prior to stimulation with lipopolysaccharide (LPS). Cells were assessed for mRNA expression of markers of microglial activation, CD11b, CD40 and intercellular adhesion molecule 1 (ICAM-1) and also the inflammatory cytokines, interleukin (IL)-1β, IL-6...

  16. Activation of AMP-activated protein kinase attenuates hepatocellular carcinoma cell adhesion stimulated by adipokine resistin

    OpenAIRE

    Yang, Chen-Chieh; Chang, Shun-Fu; Chao, Jian-Kang; Lai, Yi-Liang; Chang, Wei-En; Hsu, Wen-Hsiu; Kuo, Wu-Hsien

    2014-01-01

    Background Resistin, adipocyte-secreting adipokine, may play critical role in modulating cancer pathogenesis. The aim of this study was to investigate the effects of resistin on HCC adhesion to the endothelium, and the mechanism underlying these resistin effects. Methods Human SK-Hep1 cells were used to study the effect of resistin on intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expressions as well as NF-κB activation, and hence cell adhesion to hu...

  17. COPD和哮喘患者血清与支气管灌洗液中IL-8,SLPI,sCD14和sICAM-1含量比较%Serum and bronchial lavage fluid concentrations of IL-8, SLPI, sCD14 and sICAM-1 in patients with COPD and asthma

    Institute of Scientific and Technical Information of China (English)

    杨万勇; 陈波; 阮福旺

    2016-01-01

    目的:通过检测支气管灌洗(BAL)液与血清中趋化因子(IL-8),分泌性白细胞蛋白酶抑制剂(SLPI),可溶性细胞间粘附分子-1(sICAM-1)和sCD14含量,探讨IL-8、SLPI,sCD14和sICAM-1作为具有相似病程的哮喘和COPD患者炎症和免疫应答反应生物标志物的潜力。方法:采用酶联免疫法(ELISA)测定哮喘(n=13)与COPD (n=25)患者血清和支气管灌洗液中IL-8,SLPI,sCD14和sICAM-1含量。结果:哮喘和COPD患者BAL中IL-8和SLPI含量远高于血清中IL-8和SLPI含量,而BAL中sICAM-1和sCD14含量远低于血清中sICAM-1和sCD14含量。在测定的所有生物标志物中,COPD患者中只有BAL IL-8的浓度高于哮喘患者BAL IL-8的浓度。两组中, BAL IL-8与SLPI相关。COPD患者中,BAL sICAM-1和sCD14相关,而哮喘患者中BAL sICAM-1与FEV1/FVC相关。此外,哮喘患者中血清中SLPI与sCD14相关,且血清中sICAM-1与FEV1/FVC负相关。结论:分析特定生物标志物时,选择正确的生物流体至关重要。在测定的4个生物标志物中,COPD患者中只有BAL IL-8浓度高于哮喘患者BAL IL-8浓度。%Objectvie To quantify bronchial lavage (BAL) fluid and serum levels of chemokine (IL-8), secretory leukocyte protease inhibitor (SLPI), soluble intracellular adhesion molecules-1 (sICAM-1) and sCD14, as surrogate markers of inflamma-tory and immune response in asthma and chronic obstructive pulmonary disease (COPD) patients with similar disease duration time. Methods Biomarkers in serum and BAL fluid from asthma (n=13) and COPD (n=25) patients were detected by ELISA . Results We found that in asthma and COPD groups the concentrations of IL-8 and SLPI are significantly higher in BAL fluid than in serum, while levels of sICAM-1 and sCD14 in BAL fluid are significantly lower than in serum. Of these 4 measured bi-omarkers, only the BAL IL-8 was higher in COPD patients when compared to asthma. In both groups, BAL IL

  18. Serum vascular cell adhesion molecule-1 (VCAM1 level is elevated in colorectal cancer regardless of the tumor stage

    Directory of Open Access Journals (Sweden)

    Rumeysa Ciftci

    2016-06-01

    Full Text Available Purpose: Vascular cell adhesion molecule-1 (VCAM1 is a transmembrane glycoprotein, which is expressed on endothelium and plays role in inflammation. It is over-expressed on colorectal cancer (CRC cells and plays role in metastasis development and angiogenesis. We aimed to compare serum VCAM1 levels of CRC patients with heathy controls and evaluate its relationship with clinicopathological parameters, treatment response and overall survival (OS.Methods: The study enrolled 111 patients with histopathologically confirmed CRC followed-up in our clinic and 30 sex- and age-matched healthy controls. Pre-treatment serum VCAM1 levels were determined by the solid-phase sandwich ELISA method.Results: Metastatic disease was present in 57 patients. Forty percent of 40 metastatic patients receiving systemic therapy had partial or complete response. The median serum VCAM1 level was significantly higher in CRC patients than controls (p<0.001. In addition, serum VCAM1 level was significantly higher in diabetic CRC patients than those without diabetes (p = 0.03. There was no significant relationship between VCAM1 and other clinicopathological parameters including stage and response to systemic therapy. The median follow-up period was 12 (±8.2 months. Twenty patients were dead at the time of analysis. The presence of metastasis (p < 0.001 and elevated CEA level (p < 0.001 were factors affecting OS significantly. However, serum VCAM1 did not have a significant impact on OS (p = 0.55.Conclusion: Serum VCAM1 level is significantly elevated in CRC patients regardless of the tumor stage. However, it has no prognostic or predictive role for response to systemic therapy.

  19. Expression of mucosal addressin cell adhesion molecule 1 on vascular endothelium of gastric mucosa in patients with nodular gastritis

    Institute of Scientific and Technical Information of China (English)

    Hiroshi Ohara; Takehiko Koji; Hiroshi Nagura; Shigeru Kohno; Hajime Isomoto; Chun-Yang Wen; Chieko Ejima; Masahiro Murata; Masanobu Miyazaki; Fuminao Takeshima; Yohei Mizuta; Ikuo Murata

    2003-01-01

    AIM: The interaction of mucosal addressin cell adhesion molecule 1 (MAdCAM-1) with integrin α4β7 mediates lymphocyte recruitment into mucosa-associated lymphoid tissue (MALT). Nodular gastritis is characterized by a unique military pattern on endoscopy representing increased numbers of lymphoid follicles with germinal center, strongly associated with H pylori infection. The purpose of this study was to address the implication of the MAdCAM-1/integrin β7 pathway in NG.METHODS: We studied 17 patients with NG and H pylori infection and 19 H pylori-positive and 14 H pylori-negative controls. A biopsy sample was taken from the antrum and snap-frozen for immunohistochemical analysis of MAdCAM1 and integrin β7. In simultaneous viewing of serial sections,the percentage of MAdCAM-1-positive to von Willebrand factor-positive vessels was calculated. We also performed immunostaining with anti-CD20, CD4, CD8 and CD68 antibodies to determine the lymphocyte subsets coexpressing integrin β7.RESULTS: Vascular endothelial MAdCAM-1 expression was more enhanced in gastric mucosa with than without H pylori infection. Of note, the percentages of MAdCAM-1-positive vessels were significantly higher in the lamina propria of NG patients than in H pylori-positive controls. Strong expression of MAdCAM-1 was identified adjacent to lymphoid follicles and dense lymphoid aggregates. Integrin β7-expressing mononuclear cells, mainly composed of CD20 and CD4 lymphocytes, were associated with vessels lined with MAdCAM-1-expressing endothelium.CONCLUSION: Our results suggest that the MAdCAM-1/integrin α4β7 homing system may participate in gastric inflammation in response to H pylori-infection and contributes to MALT formation, typically leading to the development of NG.

  20. Study of the effect of atorvastatin on the interaction between ICAM-1 and CD11b by live-cell single-molecule force spectroscopy

    Institute of Scientific and Technical Information of China (English)

    2010-01-01

    The interaction between the cell adhesion molecule CD11b and its ligand ICAM-1 plays an important role in inflammatory responses in the disease of atherosclerosis. Atorvastatin is a commonly prescribed statin drug which has been considered as one of the most potent therapeutic agents for atherosclerosis due to its lipid-lowering effect. Recently, there is a growing body of evidence that atorvastatin has anti-inflammatory effect. We have applied the advanced method of live-cell single-molecule force spectroscopy to investigate the effect of atorvastatin on adhesion force between ICAM-1 and CD11b. Our result showed that single-molecule binding force of ICAM-1 and CD11b detected by AFM in the living cells was about 40 pN, and atorvastatin did not affect this force by blocking ICAM-1 or CD11b. This was different from the ICAM-1 monoclonal antibody, which could directly reduce the binding force of ICAM-1 and CD11b. Flow cytometry results revealed that atorvastatin pretreatment decreased the ICAM-1 expression in TNF-α activated HUVECs, which may contribute to its anti-inflammatory effect. The study provides a new approach to study anti-inflammatory mechanism for clinic drugs.

  1. Serum prepared with detoxication-promoting blood flow recipe on vascular endothelium cell and intercellular adhesion molecule-1 injured by oxidized low density lipoprotein%解毒活血方含药血清对氧化低密度脂蛋白损伤血管内皮细胞及细胞间黏附分子1的影响

    Institute of Scientific and Technical Information of China (English)

    贾琳; 耿立梅; 王亚利

    2013-01-01

    目的 通过观察解毒活血方含药血清(SPR)对氧化低密度脂蛋白(ox-LDL)损伤内皮细胞及细胞间黏附因子1(ICAM-1)的影响,探讨该方防治冠心病的作用机制.方法 用10只Wistar大鼠,分成两组,每组5只,分别制备空白血清和解毒活血方含药血清,然后依据细胞培养条件对提取的血清进行分组.①空白对照组:20%空白血清+5%新生牛血清(FCS)培养液;②病理模型组:20%空白血清+100 mg/L ox-LDL+5% FCS培养液;③SPR低剂量组:10% SPR+10%空白血清+100 mg/L ox-LDL+5%FCS培养液;④SPR高剂量组:20% SPR+100 mg/L ox-LDL+5%FCS培养液,每组各6个标本,共获得24个标本,分别检测各组超氧化物歧化酶(SOD)、丙二醛(MDA)、ICAM-1等指标的变化.结果 病理模型组SOD比空白对照组明显降低,加入SPR后有明显提高,SPR高剂量组比SPR低剂量组提高更多(P <0.05或<0.01),分别为(58.26±1.34) kU/L vs(65.10±1.35)kU/L,(63.57±1.63) kU/L,(67.63±2.95) kU/L.病理模型组MDA水平和ICAM-1表达与空白对照组比较明显增加,加入SPR后有明显降低,SPR高剂量组比SPR低剂量组降低更多,分别为MDA(10.02±1.66)μmol/L vs (6.68±0.82) μmol/L,(6.87±1.26) mg/L,(6.83±0.46) mg/L;ICAM-1(0.51±0.06) mg/L vs (0.37±0.05) mg/L,(0.45±0.02) mg/L,(0.40±0.04) mg/L.结论 SPR防治冠心病的机制与抗脂质过氧化、抑制或减少炎症因子ICAM-1的释放有关.%Objective The aim was to explore the mechanism of the serum prepared with detoxication-promoting blood flow recipe(SPR) in prevention of coronary heart disease, we observed the effects of this recipe on the vascular endothelium cell and intercellular adhesion molecule-1(ICAM-1) both injured by oxidized low density lipoprotein(ox-LDL).Methods Ten Wistar rats were divided into two groups,each group five rats, then the control serum and the recipe serum were prepared.According different conditions for cell culture from the serum, four groups were

  2. Influence of artificial CO2 cavity on MMP-2 and VCAM-1, ICAM-1 expression in MDA-MB-231 cell%体外模拟 CO2气腔对乳腺癌细胞 MMP-2和黏附分子 VCAM-1、ICAM-1表达的影响

    Institute of Scientific and Technical Information of China (English)

    陈琪枫; 蔡清萍; 方晓明; 姚宁; 方旭东; 龚谋春

    2015-01-01

    目的:探讨体外模拟CO2气腔对MDA-MB-231细胞基质金属蛋白酶-2( matrix metalloprotei-nase 2,MMP-2)和黏附分子血管细胞间黏附分子-1( vascular cell adhesion molecule 1,VCAM-1)、细胞间黏附分子-1(intercellular adhesion molecule 1ICAM-1)表达的影响。方法体外建立人工气腔,MDA-MB-231细胞在7 mmHg(1 mmHg=0.133 kPa)的CO2分压下暴露l、2及4 h,在处理后0、24、48及72 h,酶联免疫吸附法( enzyme linked immunosorbent assay , ELISA )测定细胞培养液中 MMP-2浓度。流式细胞术测定VCAM-1、ICAM-1表达。缺氧组选用0 mmHg的氦气(1 h)。对照组为常规培养条件。结果1、2及4 h的CO2组处理后0 h时MMP-2的表达明显高于对照组(F=15.045,P<0.05);2 h的CO2组处理后24 h时MMP-2的表达也明显高于对照组和1、4 h的CO2组(F=5.976,P<0.05)。1、2及4 h的CO2组处理后0、24 h时VCAM-1的表达显著高于对照组(F1=18.321,F2=20.443,P<0.05);4 h的CO2组处理后72 h时VCAM-1的表达显著低于1、2 h的CO2组(F=15.045,P<0.05)。缺氧组和1、2及4 h的CO2组处理后0 h时ICAM-1的表达显著高于对照组,其中2 h的CO2组表达又高于1、4 h的CO2组(F=73.765,P<0.05);2、4 h的CO2组处理后24 h时ICAM-1的表达显著高于对照组和1 h的CO2组(F=46.322,P<0.05);2 h的CO2组处理后48 h时ICAM-1的表达显著高于对照组和1、4 h的CO2组(F=22.315,P<0.05)。结论模拟7 mmHg的CO2气腔可使MDA-MB-231细胞MMP-2、VCAM-1、ICAM-1的表达增高,乳腔镜CO2气腔可能对乳腺癌细胞的转移具有一定影响力。%Objective To investigate the influence of in vitro artificial CO 2 cavity on matrix metallopro-teinase 2(MMP-2), adhesion molecule vascular cell adhesion molecule 1(VCAM-1), and intercellular adhesion molecule 1(ICAM-1)expression in MDA-MB-231 cell.Methods An in vitro artificial CO2 cavity model was es

  3. 细胞间黏附分子-1靶向微泡超声造影成像评价肾移植后急性排异反应%Ultrasound imaging of acute renal allograft rejection with microbubbles targeted to intercellular adhesion molecule-1

    Institute of Scientific and Technical Information of China (English)

    纪丽景; 王宝平; 罗利红; 吴凤林

    2011-01-01

    目的 探讨靶向超声分子成像评价肾移植后急性排异反应的可行性.方法 采用“亲和素-生物素”桥接法构建携抗细胞间黏附分子-1(ICAM-1)靶向微泡(MBI)和携同型抗体对照微泡(MB).10只SD大鼠行左侧肾异种移植术,术后72 h移植肾随机先后注入MBI和MB(间隔30 min),分别于注入3 min后行移植肾超声造影检查,并测量移植肾声强度(VI),最后进行肾组织病理及免疫组化检测.结果 移植肾在注入靶向超声微泡后可见肾区域明显灌注显影,延迟3 min显像MBI组在移植肾可见显著的超声显影增强.而MB组移植肾仅见轻度的超声显影增强,其显影强度较前者明显减弱.MBI组和MB组移植肾VI值分别为(27.0±7.4)U、(10.2±2.4)U,两者之间差异有统计学意义(F=64.744,P<0.05).结论应用靶向ICAM-1超声微泡和超声造影结合能有效评价大鼠肾移植急性排异.%Objective To assess the feasibility of evaluation of renal allograft acute rejection in rat with contrast-enhanced ultrasound ( CEUS ) and targeted microbubbles.Methods Phospholipid microbubbles targeted to intercellular adhesion molecule -1 (ICAM-1)(MBI) and control microbubbles (MB) were created by conjugating monoclonal antibody against ICAM-1 or isotype control antibody to the lipid capsule via “avidin-biotin” bridging.Ten SD rats with acute renal allograft rejection were injected intravenous of MBI and MB in random order with a 30-min interval.After 3 min of intravenous injection of microbubbles,targeted CEUS imaging was performed in all rats.And then the video intensity (VI) was determined.Results In MBI group,a significant ultrasonic enhancement was observed,but it was not very obvious in MB group.Increment in VI value of transplant kidney in MBI group was great and it amounted to (27.0 ± 7.4)U,however,increment in VI value of in MB group was minor and it was merely (10.2 ± 2.4) U,Difference was evident in transplant kidney between of the two

  4. Evaluation of C-Reactive Protein, Endothelin-1, Adhesion Molecule(s, and Lipids as Inflammatory Markers in Type 2 Diabetes Mellitus Patients

    Directory of Open Access Journals (Sweden)

    Hala El-Mesallamy

    2007-01-01

    Full Text Available This study compared lipids, the product of lipid peroxidation malondialdehyde (MDA, the acute phase reactant high sensitive C-reactive protein (hsCRP, endothelin-1 (ET-1, P-selectin, intercellular adhesion molecule-1 (ICAM-1, and vascular cell adhesion molecule-1 (VCAM-1 between healthy controls, subjects with ischemic heart disease (IHD and type 2 diabetes mellitus (DM subjects who did not perform coronary artery bypass graft (CABG surgery as well as type 2 DM subjects who performed CABG. HbA1c, lipids, MDA, hsCRP, ET-1, P-selectin, ICAM-1, and VCAM-1 levels were significantly higher in the diabetic groups than in either healthy controls or IHD subjects. In the diabetic groups, there was a negative association among hsCRP and HDL-C. ET-1, ICAM-1 levels and TAG were positively correlated, as do the association between P-selectin, VCAM-1 and HbA1c%. Also a positive relation was found among hsCRP levels and ICAM-1, as well as MDA and ET-1. P-selectin and ICAM-1 were significantly positively correlated. This study indicates that increased level of oxidative stress marker, proinflammatory markers and their downstream effectors adhesion molecules occurs in type 2 DM.

  5. Effects of curcumin on ICAM-1 expression of TNF-α-stimulated human umbilical vein endothelial cells%姜黄素对TNF-α诱导的HUVEC表达ICAM-1的调节作用

    Institute of Scientific and Technical Information of China (English)

    施颖琦; 于成功

    2014-01-01

    目的:细胞间黏附分子(intercellular adhesion molecule,ICAM)-1在炎症性肠病患者肠道炎症的发生中起着十分重要的作用.肿瘤坏死因子(tumor necrosis factor,TNF)-α可诱导内皮细胞ICAM-1的过度表达.本研究通过姜黄素干预人脐静脉内皮细胞(human umbilical vein endothelial cells,HUVEC),观察姜黄素是否能够影响TNF-α诱导ICAM-1的表达.方法:从新生儿脐带中获取HUVEC进行原代培养,取第3~5代的细胞,并将其分成3个实验组:空白对照组,不做处理;TNF-α组,加入10 ng/ml TNF-α干预3h;姜黄素组,先加入10 μmol/L姜黄素干预2h,再加入10 ng/ml TNF-α干预3h.通过流式细胞仪检测3组HUVEC细胞表面ICAM-1的表达量;同时通过免疫荧光技术观察3组细胞表达ICAM-1的荧光强度;Real-time PCR技术检测3组细胞中ICAM-1 mRNA的表达.结果:①流式细胞检测发现,TNF-α组中HUVEC表面ICAM-1的表达较空白对照组明显增加[(88.69±3.14)%vs(9.82±1.21)%,P<0.01];姜黄素组中ICAM-1表达[(41.85±8.39)%]较TNF-α组明显下降(P<0.01),但高于空白对照组(p<0.01);②免疫荧光检测也显示,TNF-α组中HUVEC细胞表面ICAM-1的表达强度明显高于空白对照组,而姜黄素组ICAM-1的表达强度较TNF-α组减弱.③Real-time PCR显示,TNF-α组中ICAM-1 mRNA的表达较空白对照组增加(34.70±14.99vs 1.03±0.26,P<0.05);姜黄素组中ICAM-1 mRNA表达(15.34±8.42)较TNF-α组下降(P<0.01),比空白对照组增加(P<0.05).结论:姜黄素可抑制TNF-α诱导的HUVEC表面ICAM-1蛋白的表达,这与其能够抑制细胞内ICAM-1 mRNA的表达有关.

  6. 早期自然流产患者蜕膜组织中ICAM-1/Mac-1的表达%Expression of ICAM-1 and Mac-1 in decidual tissues of patients with early spontaneous abortion

    Institute of Scientific and Technical Information of China (English)

    王立芹; 于学文; 张永爱; 周小兰; 褚静; 李静

    2012-01-01

    目的 通过观察细胞间黏附分子-1(ICAM-1)和巨噬细胞分化抗原-1(Mac-1)在早期自然流产患者蜕膜组织中的表达,探讨ICAM-1/Mac-1与早期自然流产的关系.方法 采用免疫组化方法检测早期自然流产患者35例和同期妊娠的30例健康妇女蜕膜组织中ICAM-1、Mac-1的表达,用激光共聚焦显微镜(CLSM)双标检测二者关系并加以分析.结果 早期自然流产患者蜕膜组织基质细胞ICAM-1、Mac-1蛋白表达强度高于对照组(Z=-3.056,P=0.002;Z=-2.132,P=0.033);流产组蜕膜腺体细胞ICAM-1、Mac-1蛋白表达强度略低于对照组(Z=-1.978,P=0.048;Z=-1.973,P=0.048);共聚焦显微镜下ICAM-1和Mac-1在早期自然流产组和对照组的蜕膜组织均有部分重叠表达.结论 ICAM-1和Mac-1在早期自然流产患者蜕膜组织基质细胞的高表达和腺体细胞的低表达可能与早期自然流产的发生有关.%Objective To explore the relationship between intracellular adhesion molecule-l( ICAM-1 )/macrophage differentiation antigen-l( Mac-1 ) and early spontaneous abortion ( SA ) by detecting the expression of ICAM-1 and Mac-1 in decidual tissues of patients with early SA. Methods The expression of ICAM-1 and Mac-1 in the deciduous tissues of 35 women with early SA and of 30 with normal abortion was detected by S-P immunohistochemistry. The relationship between ICAM-l/Mac-1 and SA was analyzed with confocal scanning laser microscope ( CLSM ). Results The expressive intensity of ICAM-1 and Mac-1 was significantly stronger in the decidual stromal cells in SA group than that in control group ( Z = -3.056, P = 0. 002; Z = -2. 132, P = 0.033 ), but the protein expressive intensity of ICAM-1 and Mac-1 in decidual glandular epithelial cells in SA group was slightly lower than that in control group ( Z = - 1. 978, P = 0. 048; Z = - 1. 973 , P =0. 048 ). The ICAM-1 and Mac-1 expression in the deciduous tissues overlapped under CLSM in both groups. Conclusion The high expression

  7. Glycyrrhizin Ameliorates Imiquimod-Induced Psoriasis-like Skin Lesions in BALB/c Mice and Inhibits TNF-a-Induced ICAM-1 Expression via NF-κB/MAPK in HaCaT Cells

    Directory of Open Access Journals (Sweden)

    Hui Xiong

    2015-02-01

    Full Text Available Background/Aim: Glycyrrhizin (GL is an important derivative of certain herbal medicines used in Asian countries. Currently, GL is used to treat hepatitis and allergic disease worldwide because of its anti-viral and anti-allergy effects. In addition to these prominent functions, GL likely regulates cellular functions such as tumor cell growth and cellular immunity. However, how GL affects the keratinocyte inflammation response remains poorly understood. The current paper investigates the effect of GL on psoriasis and explores the mechanisms involved. Methods: We used an in vitro cell model of tumor necrosis factor (TNF-a-induced keratinocyte inflammation and the topical application of imiquimod (IMQ using an animal model (mouse skin of IMQ-induced psoriasis-like inflammation (IPI to investigate the effect of GL on skin inflammation. Cell viability was analyzed using the Cell Counting Kit-8 (CCK8. Carboxyfluorescein succinimidyl ester (CFSE labeling was used to trace monocyte adherence to keratinocytes. A Western blot analysis was used to detect the expression of intercellular adhesion molecule 1 (ICAM-1 and the activation of the nuclear factor (NF-κB/mitogen-activated protein kinase (MAPK signaling pathway. A modified version of the Psoriasis Area Severity Index (PASI was used to monitor disease severity. Hematoxylin and eosin (H&E staining was used to observe pathological changes. An immunohistochemistry (IHC analysis was used to detect ICAM-1 expression in mouse skin. Results: GL treatment significantly reduced the levels of ICAM-1 in TNF-a-stimulated HaCaT cells, inhibited subsequent monocyte adhesion to keratinocytes, and suppressed the nuclear translation and phosphorylation of p65 following the degradation of inhibitor κB (IκB. GL treatment blocked the phosphorylation of extracellular signal-regulated kinase (ERK/p38 MAPK. GL effectively delayed the onset of IPI in mice and ameliorated ongoing IPI, thereby reducing ICAM-1 expression in

  8. CRP、ICAM-1与冠心病心功能的关系研究%Relationship between CRP,ICAM-1 and cardiac function in patients with coronary heart disease

    Institute of Scientific and Technical Information of China (English)

    臧金凤

    2016-01-01

    Objective:To study the relationship between the level of serum C reactive protein and intercellular adhesion molecule and the pathogenesis and progression of coronary heart disease.Methods:84 patients with coronary heart disease were selected as the coronary heart disease group,and we selected 80 normal healthy persons as the control group.Then measured CRP levels in the two groups using radioimmunoassay,and using ELISA to detect the level of ICAM-1.Results:The level of serum CRP and ICAM-1 in the CHD group were significantly higher than those in the control group(P<0.05).With the increasing of gensini score in patients with coronary heart disease,the level of CRP and ICAM-1 were significantly raised(P<0.05).Conclusion:CRP and ICAM-1 have closely relationship with the incidence of coronary heart disease and disease progression,so it can be used as indicators to evaluate the prognosis of coronary heart disease.%目的:探讨血清C反应蛋白及胞间黏附分子水平与冠心病发病及病情进展的关系。方法:收治冠心病患者84例为冠心病组,另选取80例正常体检者为对照组,应用放射免疫法测定两组CRP水平,ELISA法测定ICAM-1水平。结果:冠心病组血清 CRP、ICAM-1水平高于对照组(P<0.05),随着冠心病患者 Gensini 评分的增高,患者CRP、ICAM-1水平升高(P<0.05)。结论:CRP、ICAM-1与冠心病发病及病情进展有密切的关系,CRP、ICAM-1水平可作为评价冠心病预后的指标。

  9. 银杏叶提取物对大鼠急性缺血心肌细胞间黏附分子-1和白细胞介素-6表达的影响%Effects of ginkgo biloba extract on intercellular adhesion molecule-1 and interleukin-6 in acute is chemic myocardium of Rats

    Institute of Scientific and Technical Information of China (English)

    黄陆力; 王崇军; 付庆林; 韩培立; 张新中; 刘永强; 王丽娜; 崔勤涛; 周朝元

    2012-01-01

    心肌损伤的程度和冠脉病变范围.(2)大鼠急性心肌梗死中应用银杏叶提取物干预,可下调心肌中ICAM-1和IL-6的表达,减轻大鼠心肌损伤程度,证实银杏叶提取物有较好的心肌保护作用.%Objective To study the expressiou of intercellular adhesion molecule-1 (ICAM-1) and interleukin (IL)-6 in myocardium with acute myocardial infarction in rats and the influence of ginkgo biloba extract on them,and to explore the mechanism of protective effects of ginkgo biloba extract on acute infarcted myocardium.Methods One hundred and nine healthy female SD rats were selected to make acute myocardial infartion model by ligation of the left anterior descending (LAD) coronary artery,and then they were randomly divided into model group ( group A,n =38 ),ginkgo biloba treatment group ( group B,n =39 ),and sham operation group ( group C,n =32).In goup A,the left anterior descending (LAD) coronary artery was ligated solely; in group B,Ginkgo biloba extract (2 mg/kg body weight) was intravenously injected 30 min before ligation of LAD coronary artery; in group C,a loose knol was made around the first descending branch of LAD coronary arterv,witbout ligation.Each group was then randomly divided into 4 subgroups,which were observed 2 h,6 h,48 h,and 7 days after operation,respectively.Blood and heart samples were collected at every time point.Morphological changes were observed by HE staining method under the light microscopy,and ICAM-1 and IL-6 expression was detected by using immunohistochemistry.Results By using HE staining,in group A,the number of myocardial cells was decreased,and myocardial interstitial congestion,edema,myocardial fiber dissolution,flaky necrosis and infiltration of inflammatory cells were observed.Range of myocardial infarction was more than 1/2 of cardiac wall,and large number of viable myocardial cells still could be seen in the other side of cardiac wall; In group B,myocardial injuries were significantly milder than

  10. Potent anti-inflammatory effect of dioscin mediated by suppression of TNF-α-induced VCAM-1, ICAM-1and EL expression via the NF-κB pathway.

    Science.gov (United States)

    Wu, Shan; Xu, Hui; Peng, Jinyong; Wang, Changyuan; Jin, Yue; Liu, Kexin; Sun, Huijun; Qin, Jianhua

    2015-03-01

    The modulation of adhesion molecule expression and the reduction of aberrant leukocyte adhesion to the endothelium are attractive approaches for treating inflammation-related vascular complications, including atherosclerosis. Dioscin has a variety of biological activities including anti-inflammatory activity. However, the molecular mechanisms behind dioscin's anti-inflammatory effects are not fully understood. In this study, we investigated the molecular mechanism involved in the effects of dioscin on inflammatory mediators in tumor necrosis factor-α (TNF-α)-stimulated human umbilical vein endothelial cells (HUVECs). In vitro, dioscin decreased monocyte adhesion to TNF-α-treated HUVECs by reducing vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) expression and inhibiting endothelial lipase (EL) expression in TNF-α-treated HUVECs and macrophages by blocking the nuclear factor-κB (NF-κB) pathway. Thus, dioscin might inhibit inflammation by interrupting the NF-κB signaling pathway and could potentially contribute to treatments for inflammatory diseases and atherosclerosis. PMID:25577996

  11. Mild hypothermia effects on intercellular adhesion molecule-1 and serum interleukin-6 expression in brain tissues of a rat focal ischemia model

    Institute of Scientific and Technical Information of China (English)

    Shengqi Fu; Lei Yang; Shuling Zhang; Shilong Sun; Xingai Mao

    2008-01-01

    BACKGROUND: Previous studies have confirmed the neuroprotective effect of mild hypothermia on ischemic brain injury.OBJECTIVE: To investigate the effects of mild hypothermia on intercellular adhesion molecule-1 expression and serum interleukin-6 levels in ischemic brain tissues of focal brain ischemia rats, and to explore the neuroprotective effects of mild hypothermia on ischemic brain injury.DESIGN, TIME AND SETTING: A randomized, controlled, neurobiological experiment was performed at the Central Laboratory, First Affiliated Hospital, Xinxiang Medical College, China from February to July 2006.MATERIALS: Thirty healthy, adult, Sprague Dawley rats were used to establish middle cerebral artery occlusion models using the suture method. The immunohistochemistry (streptavidin-biotin-peroxidase complex method) kit was purchased from Boster, China. Interleukin-6 radioimmunoassay was supplied by Institute of Radioimmunity, Technology Development Center, General Hospital of Chinese PLA. METHODS: The rats were equally and randomly assigned into mild hypothermia and control groups, and middle cerebral artery occlusion models were established. The rectal temperature was maintained at (37 ± 0.5)℃ in the control group. In the mild hypothermia group, the rectal temperature was maintained at (33±1)℃.MAIN OUTCOME MEASURES: At 12 hours after model establishment, the ischemic brain hemispheres were coronally sliced at the level of the optic chiasm. The number of intercellular adhesion molecule- 1 -positive vessels per high-power field was observed with an optical microscope. Serum interleukin-6 levels were measured by radioimmunoassay.RESULTS: Compared with the control group, intercellular adhesion molecule-I and serum interleukin-6 expressions were significantly decreased in ischemic brain tissues of the mild hypothermia group (P < 0.01).CONCLUSION: Mild hypothermia exhibits a neuroprotective effect by reducing serum interleukin-6 and intercellular adhesion molecule- 1

  12. ICAM-1 and AMPK regulate cell detachment and apoptosis by N-methyl-N Prime -nitro-N-nitrosoguanidine, a widely spread environmental chemical, in human hormone-refractory prostate cancers

    Energy Technology Data Exchange (ETDEWEB)

    Chen, Yi-Cheng; Lu, Pin-Hsuan; Hsu, Jui-Ling; Yu, Chia-Chun; Guh, Jih-Hwa, E-mail: jhguh@ntu.edu.tw

    2011-12-15

    Poly(ADP-ribose) polymerase-1 (PARP-1), a sensor of DNA damage, plays a crucial role in the regulation of DNA repair. PARP-1 hyperactivation causes DNA damage and cell death. The underlying mechanism is complicated and is through diverse pathways. The understanding of responsible signaling pathways may offer implications for effective therapies. After concentration-response determination of N-Methyl-N Prime -Nitro-N-Nitrosoguanidine (MNNG, a PARP-1 activating agent and an environmental mutagen) in human hormone-refractory prostate cancers, the data showed that concentrations below 5 {mu}M did not change cell survival but cause a time-dependent up-regulation of intracellular adhesion molecule-1 (ICAM-1) in mRNA, total protein and cell surface levels. Detection of phosphorylation and degradation of I{kappa}B-{alpha} and nuclear translocation of NF-{kappa}B showed that MNNG induced the activation of NF-{kappa}B that was responsible for the ICAM-1 up-regulation since PDTC (a NF-{kappa}B inhibitor) significantly abolished this effect. However, higher concentrations (e.g., 10 {mu}M) of MNNG induced a 61% detachment of the cells which were apoptosis associated with the activation of AMP-activated protein kinase (AMPK), c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK). Further identification showed that both AMPK and JNK other than p38 MAPK functionally contributed to cell death. The remaining 39% attached cells were survival associated with high ICAM-1 expression. In conclusion, the data suggest that NF-{kappa}B-dependent up-regulation of ICAM-1 plays a key role on cell attachment and survival; whereas, activation of AMPK and JNK participates in cytotoxic signaling pathways in detached cells caused by PARP-1 activation. Highlights: Black-Right-Pointing-Pointer Low level of DNA damage helps cell attachment and survival via ICAM-1 upregulation. Black-Right-Pointing-Pointer High level of DNA damage causes AMPK- and JNK-involved cell detachment

  13. Child hospitalization due to severe malaria is associated with the ICAM-1(Kilifi) allele but not adherence patterns of Plasmodium falciparum infected red blood cells to ICAM-1

    NARCIS (Netherlands)

    Mwanziva, C.; Mpina, M.; Balthazary, S.; Mkali, H.; Mbugi, E.V.; Mosha, F.; Chilongola, J.

    2010-01-01

    This study aimed at determining whether the predisposition of a mutation at position 179 of the ICAM-1 gene to child hospitalization due to malaria was mediated by changes in adherence properties of IRBCs to ICAM-1. ICAM-1 genotypes were determined by nested polymerase chain reaction of isolated DNA

  14. Different Doses of Febuxostat and Allopurinol Influencing Soluble Intercellular Adhesion Molecule 1 in Patients with Hy-peruricemia Complicated by Gout%不同剂量非布司他与别嘌呤醇对高尿酸血症伴痛风患者可溶性细胞间黏附分子1影响的对比观察

    Institute of Scientific and Technical Information of China (English)

    沈赟; 金星; 陶沙; 蒋兰兰; 吴锦丹

    2014-01-01

    Objective To explore the influence of febuxostat and allopurinol on soluble intercellular adhesion molecule 1(sICAM -1)in patients with hyperuricemia complicated by gout. Methods Sixty patients with hyperuricemia and gout admitted to Nanjing Hospital from June to October 2010 were randomly divided into group A,B,C,20 in each. Group A administered 40 mg febuxostat,1 piece/ time,1 time/ d;group B given 80 mg febuxostat,1 piece/ time,1 time/ d;group C had 300 mg allopurinol tablets,1 piece/ time,3 times/ d. The courses lasted 24 weeks. The serum sICSM - 1,uric acid( UA) levels were determined before treatment,in weeks 12,24 after treatment. Results In intra - class comparison,there were significant differences in sICAM -1,UA levels in 3 groups before treatment,in weeks 12,24(P ﹤0. 05);in group comparison, there was no significant difference in 3 groups(P ﹥0. 05). Pearson correlation analysis showed that serum sICAM -1 was positively correlated with UA(r =0. 248,P = 0. 007). Conclusion 40 mg,80 mg febuxostat and allopurinol can reduce serum sICAM -1,UA levels in patients with hyperuricemia complicated by gout,which may play an active role in improving inflammation ,protecting vascular endothelial cell function.%目的:对比不同剂量非布司他与别嘌呤醇对高尿酸血症伴痛风患者血清可溶性细胞间黏附分子1(sICAM-1)水平的影响,探讨其抗炎作用。方法选取2010年6-10月在南京医科大学附属医院门诊就诊的高尿酸血症伴痛风(缓解期)患者60例,采用随机数字表法将患者分为A组、B组、C组,每组20例。A组患者服用40 mg非布司他片,1片/次,1次/d;B组患者服用80 mg非布司他片,1片/次,1次/d;C组患者服用300 mg别嘌呤醇片,1片/次,3次/d。3组患者均连续治疗24周。检测3组患者治疗前及治疗12周、治疗24周时血清sICAM-1、尿酸水平。结果组内比较,3组患者治疗前及治疗12周、治疗24周时血清sICAM-1

  15. sICAM- 1 and sVCAM- 1 levels in blood serum and gingival tissues in rabbits with periodontitis in analogic high altitude anoxia environment%模拟高原低氧兔牙周炎模型血清和牙龈组织中sICAM-1及sVCAM-1的含量

    Institute of Scientific and Technical Information of China (English)

    武曦; 黄镜静; 张纲; 谭颖徽; 高钰琪

    2012-01-01

    Objective: To investigate the expression of soluble inter-cellular adhesion molecules-1( sICAM-1 ) and soluble vascular adhesion molecular-1( sVCAM-1 ) in blood serum and gingival tissues in rabbits with periodontitis in high altitude anoxia environment. Methods: 40 male rabbits were randomly divided into four groups( n = 10 ): control and periodontitis groups in plain, control and periodontitis groups in plateau. The periodontitis models were established by ligation technique on the two central incisors of mandible and periodontitis diet. The anoxia groups were raised in a established condition of altitude at 5 000 meteres above sea level for eight weeks. sICAM-1 and sVCAM-1 levels in blood serum and gingival tissues were detected by ELISA. The morphology of the periodontal tissues were histologicaly observed. Results: More severe periodontitis was observed in anoxia periodontits groups. The concentrations of sl-CAM-1 and sVCAM-1 in anoxia periodontitis group were significantly higher than those in the other groups( P <0. 05 ), and the levels in gingival tissues were higher in blood serum. Conclusion: Cellular adhesion molecules are upregulated in anoxia environment at high altitude and may promotes the destruction of periodontal tissues and diffusion of inflammation into the peripheral blood vessels.%目的:探讨血清和牙龈组织中可溶性细胞间黏附分子- 1(sICAM- 1)、可溶性血管黏附分子- 1(sVCAM- 1)在高原牙周病炎症反应中的作用.方法:将40 只雄兔随机分为常氧对照组、常氧实验组、低氧对照组、低氧实验组,每组10 只,采用正畸丝结扎下颌中切牙与牙周炎食谱的方法建立牙周炎模型,常氧组和低氧组分别在平原和模拟海拔5 000 m条件下饲养8 周,对牙周组织取材进行组织学观察,用ELISA法检测各组实验动物血清和牙龈组织中sICAM- 1、sVCAM- 1表达情况.结果:低氧实验组sICAM- 1、sVCAM- 1浓度显著高于其余各组(P<0.05),且牙龈组

  16. 糖基化终产物刺激大鼠骨髓内皮细胞表达细胞间粘附分子-1的机制探讨%The mechanism of intercellular adhesion molecule-1 expression in endothelial cells stimulated by advanced glycosylation end products

    Institute of Scientific and Technical Information of China (English)

    余路; 邱鸿鑫; 王亚平; 司良毅; 吴珊; 祝继华

    2001-01-01

    AIM: To explore the relationship between intercellular adhesionmolecule-1(ICAM-1)expression in endothelial cells(EC) and advanced glycosylation end products(AGEs) stimulation. METHODS: Murine bone marrow derived ECs was stimulated by AGEs after pretreated with anti-AGEs, anti-IL-1β and N-acetylcysteine(NAC),then SOD activity and ICAM-1 concentration and adhesion rate(AR) were evaluated. RESULTS: ECs which expressed ICAM-1[(0.65±0.14) vs (0.11±0.02)] induced by AGEs showed lower SOD activity [(0.69±0.19)×103 U/L vs (1.71±0.42)×103 U/L]. The ICAM-1 expression as well as the increase of AR caused by AGEs stimulation could be suppressed by anti-AGEs(0.12±0.01) and NAC(0.11±0.05). Anti-IL-1β had no influence on these changes. CONCLUSION: AGEs could induce endothelial cells to express ICAM-1 in vitro, most probably due to the formation of free radicals. Besides, AGEs may stimulate other cells to secrete cytokines resulting in ICAM-1 expression in endothelial cells.%目的:探讨糖基化终产物(AGEs)致内皮细胞表达细胞间粘附分子-1(ICAM-1)与自由基产生之间的关系。方法:内皮细胞(EC)用抗AGEs抗体、抗IL-1β多抗、N-乙酰半胱氨酸(NAC)预处理1h后AGEs作用6h,测定IL-1β、超氧化物歧化酶(SOD)、ICAM-1、内皮细胞-中性粒细胞粘附率。结果:AGEs刺激后ICAM-1表达增加[吸光度(A)为0.65±0.14vs0.11±0.02]的内皮细胞SOD活性降低[(0.69±0.19)×103U/Lvs(1.71±0.42)×103U/L]。ICAM-1的增加可被抗AGEs抗体[吸光度(A)为(0.12±0.01)]、NAC[吸光度(A)为(0.11±0.05)]和抗ICAM-1抗体[吸光度(A)为(0.10±0.04)]抑制。外源性IL-1β也可刺激内皮细胞表达ICAM-1[吸光度(A)为(0.72±0.23)]。结论:AGEs刺激内皮细胞表达ICAM-1可能与其导致细胞自由基的产生有关;AGEs还可通过刺激其他细胞产生细胞因子间接作用于EC,参与促进ICAM-1表达。

  17. Cytokine and adhesion molecule expression evolves between the neutrophilic and lymphocytic phases of viral meningitis.

    Science.gov (United States)

    Makis, Alexandros; Shipway, David; Hatzimichael, Eleftheria; Galanakis, Emmanouil; Pshezhetskiy, Dmitry; Chaliasos, Nikolaos; Stebbing, Justin; Siamopoulou, Antigone

    2010-09-01

    Viral meningitis is characterized by cerebrospinal fluid (CSF) lymphocyte pleocytosis, although neutrophils may predominate in the early phase. The T helper 1 (Th1)/Th2 cytokine balance and expression of adhesion molecules seem to be involved in the CSF chemotaxis. We aimed to determine expression of cytokines and adhesion molecules in enteroviral meningitis. We investigated the serum and CSF levels of adhesion molecules (E-selectin, L-selectin, vascular cell adhesion molecule-1 [VCAM-1], and intracellular adhesion molecule-1 [ICAM-1]) and cytokines (interleukin-12 [IL-12] and IL-4) in 105 children during an outbreak of enteroviral meningitis. Diagnosis was confirmed with positive polymerase chain reaction (PCR) and/or serology for echovirus or Coxsackie virus, and matched with control subjects for clinical features but with negative PCR and/or serology. Apart from VCAM-1, the CSF levels of all investigated inflammatory molecules were significantly increased. In serum, sL-selectin and ICAM-1 levels were significantly higher than control subjects. Serum and CSF L-selectin, serum VCAM-1, and CSF IL-12 were all observed to be expressed in significantly higher levels in the neutrophil-dominant subgroup (72% had duration of symptoms 24 h). Serum and CSF ICAM-1 was found at significantly higher levels in the latter group. Evolving expression of adhesion molecules and cytokines indicates a shift from Th1 to Th2 immune responses as infection progresses.

  18. The neutrophil-specific antigen CD177 is a counter-receptor for platelet endothelial cell adhesion molecule-1 (CD31).

    Science.gov (United States)

    Sachs, Ulrich J H; Andrei-Selmer, Cornelia L; Maniar, Amudhan; Weiss, Timo; Paddock, Cathy; Orlova, Valeria V; Choi, Eun Young; Newman, Peter J; Preissner, Klaus T; Chavakis, Triantafyllos; Santoso, Sentot

    2007-08-10

    Human neutrophil-specific CD177 (NB1 and PRV-1) has been reported to be up-regulated in a number of inflammatory settings, including bacterial infection and granulocyte-colony-stimulating factor application. Little is known about its function. By flow cytometry and immunoprecipitation studies, we identified platelet endothelial cell adhesion molecule-1 (PECAM-1) as a binding partner of CD177. Real-time protein-protein analysis using surface plasmon resonance confirmed a cation-dependent, specific interaction between CD177 and the heterophilic domains of PECAM-1. Monoclonal antibodies against CD177 and against PECAM-1 domain 6 inhibited adhesion of U937 cells stably expressing CD177 to immobilized PECAM-1. Transendothelial migration of human neutrophils was also inhibited by these antibodies. Our findings provide direct evidence that neutrophil-specific CD177 is a heterophilic binding partner of PECAM-1. This interaction may constitute a new pathway that participates in neutrophil transmigration. PMID:17580308

  19. Role of NF-κB-p65, ICAM-1 and apoptosis in exhausted exercise-induced delayed-onset myocardial injury%NF-κB-p65、ICAM-1和细胞凋亡在力竭性运动诱发延迟性心肌损伤中的作用

    Institute of Scientific and Technical Information of China (English)

    王春晓; 梁玉记; 王燕; 胡志力; 王福文

    2013-01-01

    目的:观察反复力竭性游泳运动后,不同时相大鼠心肌组织中核转录因子-κB(NF-κB)-p65、细胞间黏附因子-1(ICAM-1)和细胞凋亡的动态变化,以评价在运动延迟性心肌损伤中的作用.方法:采用反复力竭性游泳运动建立延迟性心肌损伤大鼠模型.将无训练的80只Wistar雄性大鼠随机分为安静对照组和反复力竭性运动后即刻组、3h组、6h组、12 h组、24h组、48 h组和96 h组.每组10只大鼠(n=10).分别于末次运动后即刻、3、6、12、24、48 h和96 h快速取出心脏,应用免疫组化染色法和DNA原位末端标记(TUNEL)法检测大鼠心肌组织中NF-κB-p65和ICAM-1表达的水平和细胞凋亡的动态变化.结果:与安静对照组比较,反复力竭性运动后不同时相大鼠心肌细胞中NF-κB-p65和ICAM-1蛋白的表达及细胞凋亡指数均显著增加(分别为P<0.05和P<0.01),其中心肌细胞中NF-κB-p65的表达和细胞凋亡于运动后48 h达高峰,ICAM-1蛋白的表达于运动后即刻达高峰,运动后96 h有所减轻.结论:反复力竭性运动可以造成早期心肌缺血缺氧损伤,刺激心肌细胞中NF-κB-p65和ICAM-1表达的水平的升高,促进炎症反应,并诱导心肌细胞凋亡,进一步加重运动后早期心肌损伤,诱发延迟性心肌损伤.%AIM: To investigate the dynamic changes of nuclear transcription factor-kappa B ( NF-κB ) p65, intracellular adhesion molecule-1 (ICAM-1) and apoptosis in myocardium of rats at different time periods after repeated exhausted exercise and to explore their roles in the development of exercise-induced delayed-onset myocardial injury. METHODS: The animal model of delayed-onset myocardial injury was established by repeated exhaustive swimming. Eighty male Wistar rats were divided randomly into sedentary control group and exhausted exercise groups, namely, 3-, 6-, 12-, 24-, 48- and 96-h groups. Rat hearts were rapidly excised at respective time points of 3-, 6-, 12-, 24-, 48

  20. 脑通汤对VD大鼠海马CA1区ICAM-1、EBA及GFAP蛋白表达的影响%Effect of Nao Tong Decoction on the ICAM-1 and EBA Expression in the Hippocampus Area of Vascular Dementia Rats

    Institute of Scientific and Technical Information of China (English)

    宋先红; 况时祥

    2015-01-01

    Objective:To observe the effects of Naotong decoction on the ability of learning and memory, and the levels of intercellular adhesion molecule 1(ICAM-1), endothelial barrier antigen (EBA),glial fibers acidic protein (GFAP) expression of hippocampal CA1 area in rats with vascular dementia, and to explore the possible therapeutic mechanism. Method: Ninety female SD rats were randomly divided into six groups: ①pseudo-operation group ②model group③Donepezil HCL group ④Naotong decoction high dose group⑤Naotong decoction moderate dose group⑥Naotong decoction low dose group, Fifteen rats contained in each group. Model making was performed on the rats in addition to the pseudo-operation group by modified Pulsinelli 4 vascular occlusions method(4VO).One week after the surgery, the rats underwent gavage treatment for 4 weeks, one time a day.Afterthe treatment, the Morris Water Maze were used to test the ability of learning and memory in vascular dementia model rats,mmunohistochemical method to detect the ICAM-1, EBA and GFAP protein expression in hippocampal CA1 area. Result: Compared to pseudo-operation group, the model group escape time were increased and the times of spanning the previous platform were reduced, the expression of ICAM-1、GFAP were reduced,and the expression of EBA were decreased(P<0.01). Compared to model group, escape time were reduced, the levels of ICAM-1、GFAP were decreased, the expression of EBA were increased in the Naotong decoction high and moderate dose groups(P<0.01).Conclusion:Naotong Decoction can obviously prevent learning and memory deficit of VaD rats,and the mechanism might relate to reduce the expression of ICAM-1 and GFAP protein, improve the EBA expression, relieve the damage to cerebral microvascular endothelial cells and astrocytes , and thus reduce ischemic damage to nerve vascular unit.%目的:观察脑通汤对血管性痴呆大鼠学习记忆能力以及海马CA1区细胞间黏附分子(ICAM-1)、内皮屏障抗

  1. Nanoscale Imaging Reveals a Tetraspanin-CD9 Coordinated Elevation of Endothelial ICAM-1 Clusters.

    Directory of Open Access Journals (Sweden)

    Jonas Franz

    Full Text Available Endothelial barriers have a central role in inflammation as they allow or deny the passage of leukocytes from the vasculature into the tissue. To bind leukocytes, endothelial cells form adhesive clusters containing tetraspanins and ICAM-1, so-called endothelial adhesive platforms (EAPs. Upon leukocyte binding, EAPs evolve into docking structures that emanate from the endothelial surface while engulfing the leukocyte. Here, we show that TNF-α is sufficient to induce apical protrusions in the absence of leukocytes. Using advanced quantitation of atomic force microscopy (AFM recordings, we found these structures to protrude by 160 ± 80 nm above endothelial surface level. Confocal immunofluorescence microscopy proved them positive for ICAM-1, JAM-A, tetraspanin CD9 and f-actin. Microvilli formation was inhibited in the absence of CD9. Our findings indicate that stimulation with TNF-α induces nanoscale changes in endothelial surface architecture and that--via a tetraspanin CD9 depending mechanism--the EAPs rise above the surface to facilitate leukocyte capture.

  2. ICAM1 and fibrinogen-γ are increased in uterine epithelial cells at the time of implantation in rats.

    Science.gov (United States)

    Lecce, Laura; Kaneko, Yui; Madawala, Romanthi J; Murphy, Christopher R

    2011-05-01

    Uterine epithelial cells transform into a receptive state to adhere to an implanting blastocyst. Part of this transformation includes the apical concentration of cell adhesion molecules at the time of implantation. This study, for the first time, investigates the expression of ICAM1 and fibrinogen-γ (FGG) in uterine epithelial cells during normal pregnancy, pseudopregnancy and in hormone-treated rats. An increase (P FGG dimerization increased (P FGG in the uterine epithelium at the time of implantation in the rat is similar to that seen in lymphocyte-endothelium adhesion, and we suggest a similar mechanism in embryo-uterine epithelium adhesion is utilized.

  3. Plasma concentrations of VCAM-1 and ICAM-1 are elevated in patients with Type 1 diabetes mellitus with microalbuminuria and overt nephropathy

    DEFF Research Database (Denmark)

    Clausen, P; Jacobsen, P; Rossing, K;

    2000-01-01

    and diabetic nephropathy are associated with elevated plasma concentrations of soluble vascular adhesion molecule (sVCAM)-1, soluble intercellular adhesion molecule (sICAM)-1, and soluble E-selectin (sE-selectin) aiming to illustrate factors of potential pathogenetic relevance for the excess cardiovascular...... with microalbuminuria (n = 15); group 3-patients with macroalbuminuria and normal serum creatinine (n = 15), group 4-patients with macroalbuminuria and moderately elevated serum creatinine (n = 13). RESULTS: Plasma concentrations of sVCAM-1 and sICAM-1 were similar in healthy controls and normoalbuminuric Type 1...... diabetic patients, but the concentrations were increased by the presence of microalbuminuria and overt nephropathy (P ICAM-1 is elevated in Type 1...

  4. Omentin inhibits TNF-{alpha}-induced expression of adhesion molecules in endothelial cells via ERK/NF-{kappa}B pathway

    Energy Technology Data Exchange (ETDEWEB)

    Zhong, Xia, E-mail: zhongxia1977@126.com [Department of Emergency, Provincial Hospital Affiliated to Shandong University, Jinan 250021 (China); Li, Xiaonan; Liu, Fuli; Tan, Hui [Department of Emergency, Provincial Hospital Affiliated to Shandong University, Jinan 250021 (China); Shang, Deya, E-mail: wenhuashenghuo1@163.com [Department of Emergency, Provincial Hospital Affiliated to Shandong University, Jinan 250021 (China)

    2012-08-24

    Highlights: Black-Right-Pointing-Pointer Omentin inhibited TNF-{alpha}-induced adhesion of THP-1 cells to HUVECs. Black-Right-Pointing-Pointer Omentin reduces expression of ICAM-1 and VCAM-1 induced by TNF-{alpha} in HUVECs. Black-Right-Pointing-Pointer Omentin inhibits TNF-{alpha}-induced ERK and NF-{kappa}B activation in HUVECs. Black-Right-Pointing-Pointer Omentin supreeses TNF-{alpha}-induced expression of ICAM-1 and VCAM-1 via ERK/NF-{kappa}B pathway. -- Abstract: In the present study, we investigated whether omentin affected the expression of intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in tumor necrosis factor-{alpha} (TNF-{alpha}) induced human umbilical vein endothelial cells (HUVECs). Our data showed that omentin decreased TNF-{alpha}-induced expression of ICAM-1 and VCAM-1 in HUVECs. In addition, omentin inhibited TNF-{alpha}-induced adhesion of THP-1 cells to HUVECs. Further, we found that omentin inhibited TNF-{alpha}-activated signal pathway of nuclear factor-{kappa}B (NF-{kappa}B) by preventing NF-{kappa}B inhibitory protein (I{kappa}B{alpha}) degradation and NF-{kappa}B/DNA binding activity. Omentin pretreatment significantly inhibited TNF-{alpha}-induced ERK activity and ERK phosphorylation in HUVECs. Pretreatment with PD98059 suppressed TNF-{alpha}-induced NF-{kappa}B activity. Omentin, NF-kB inhibitor (BAY11-7082) and ERK inhibitor (PD98059) reduced the up-regulation of ICAM-1 and VCAM-1 induced by TNF-{alpha}. These results suggest that omentin may inhibit TNF-{alpha}-induced expression of adhesion molecules in endothelial cells via blocking ERK/NF-{kappa}B pathway.

  5. TWEAK enhances E-selectin and ICAM-1 expression, and may contribute to the development of cutaneous vasculitis.

    Directory of Open Access Journals (Sweden)

    Tao Chen

    Full Text Available Our previous work indicated that TWEAK is associated with various types of cutaneous vasculitis (CV. Herein, we investigate the effects of TWEAK on vascular injury and adhesion molecule expression in CV mice. We showed that TWEAK priming in mice induced a local CV. Furthermore, TWEAK priming also increased the extravasation of FITC-BSA, myeloperoxidase activity and the expression of E-selectin and ICAM-1. Conversely, TWEAK blockade ameliorated the LPS-induced vascular damage, leukocyte infiltrates and adhesion molecules expression in LPS-induced CV. In addition, TWEAK treatment of HDMECs up-regulated E-selectin and ICAM-1 expression at both mRNA and protein levels. TWEAK also enhanced the adhesion of PMNs to HDMECs. Finally, western blot data revealed that TWEAK can induce phosphorylation of p38, JNK and ERK in HDMECs. These data suggest that TWEAK acted as an inducer of E-selectin and ICAM-1 expression in CV mice and HDMECs, may contribute to the development of CV.

  6. Expression of adhesion molecules on mature cholangiocytes in canal of Hering and bile ductules in wedge biopsy samples of primary biliary cirrhosis

    Institute of Scientific and Technical Information of China (English)

    Hiroaki Yokomori; Toshifumi Hibi; Masaya Oda; Mariko Ogi; Go Wakabayashi; Shigeyuki Kawachi; Kazunori Yoshimura; Toshihiro Nagai; Masaki Kitajima; Masahiko Nomura

    2005-01-01

    AIM: To examine the expression of intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1) expression on canals of Hering (CoH)and bile ductules associated with the autoimmune process of bile duct destruction in primary biliary cirrhosis (PBC).METHODS: Ten wedged liver biopsies of PBC (five cases each of stages 2 and 3) were studied. The liver specimens were processed for transmission electron microscopy.Immunohistochemistry was performed using anti-ICAM-1 and anti-LFA-1 mouse mAbs. In situ hybridization was done to examine the messenger RNA expression of ICAM-1 in formalin-fixed, paraffin-embedded sections using peptide nucleic acid probes and the catalyzed signal amplification (CSA) technique. Immunogold-silver staining for electron microscopy was performed using anti-ICAM and anti-LFA-1 mouse mAbs. The immunogold particles on epithelial cells of bile ductules and cholangiocytes of CoH cells were counted and analyzed semi-quantitatively.Western blotting was performed to confirm ICAM-1 protein expression.RESULTS: In liver tissues of PBC patients, immunohistochemistry showed aberrant ICAM-1 expression on the plasma membrane of epithelial cells lining bile ductules,and also on mature cholangiocytes but not on hepatocytes in CoH. LFA-1-positive lymphocytes were closely associated with epithelial cells in bile ductules. ICAM-1 expression at protein level was confirmed by Western blot. In situ hybridization demonstrated ICAM-1 mRNA expression in bile ductules and LFA-1 mRNA in lymphocytes infiltrating the bile ductules. By immunoelectron microscopy, ICAM-1 was demonstrated on the basal surface of epithelial cells in bile ductules and on the luminal surfaces of cholangiocytes in damaged CoH. Cells with intermediate morphology resembling progenitor cells in CoH were not labeled with ICAM-1 and LFA-1.CONCLUSION: De novo expression of ICAM-1 both on mature cholangiocytes in CoH and epithelial cells in bile ductules in PBC implies that

  7. Short-term high-fat diet alters postprandial glucose metabolism and circulating vascular cell adhesion molecule-1 in healthy males.

    Science.gov (United States)

    Numao, Shigeharu; Kawano, Hiroshi; Endo, Naoya; Yamada, Yuka; Takahashi, Masaki; Konishi, Masayuki; Sakamoto, Shizuo

    2016-08-01

    Short-term intake of a high-fat diet aggravates postprandial glucose metabolism; however, the dose-response relationship has not been investigated. We hypothesized that short-term intake of a eucaloric low-carbohydrate/high-fat diet (LCHF) would aggravate postprandial glucose metabolism and circulating adhesion molecules in healthy males. Seven healthy young males (mean ± SE; age: 26 ± 1 years) consumed either a eucaloric control diet (C, approximately 25% fats), a eucaloric intermediate-carbohydrate/intermediate-fat diet (ICIF, approximately 50% fats), or an LCHF (approximately 70% fats) for 3 days. An oral meal tolerance test (MTT) was performed after the 3-day dietary intervention. The concentrations of plasma glucose, insulin, glucagon-like peptide-1 (GLP-1), intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 (VCAM-1) were determined at rest and during MTT. The incremental area under the curve (iAUC) of plasma glucose concentration during MTT was significantly higher in LCHF than in C (P = 0.009). The first-phase insulin secretion indexes were significantly lower in LCHF than in C (P = 0.04). Moreover, the iAUC of GLP-1 and VCAM-1 concentrations was significantly higher in LCHF than in C (P = 0.014 and P = 0.04, respectively). The metabolites from ICIF and C were not significantly different. In conclusion, short-term intake of eucaloric diet containing a high percentage of fats in healthy males excessively increased postprandial glucose and VCAM-1 concentrations and attenuated first-phase insulin release. PMID:27454856

  8. 西洛他唑联合替米沙坦对早期2型糖尿病肾病血清单核细胞趋化蛋白1和可溶性细胞间黏附分子1的影响%The Effect of Cilostazol Combined with Telmisartan on Serum Monocyte Chemotactic Protein-1 and Soluble Intercellu-lar Adhesion Molecule-1 in Early Type 2 Diabetic Nephropathy

    Institute of Scientific and Technical Information of China (English)

    焦秀敏; 武晋晓; 陈彬; 袁涛; 吕肖锋

    2014-01-01

    Objective To observe the effect of cilostazol combined with telmisartan on serum monocyte chemotactic pro-tein-1 (MCP-1) and soluble intercellular adhesion molecule-1 (sICAM-1) in early type 2 diabetic nephropathy. Methods A total of 60 patients with early type 2 diabetic nephropathy were randomly divided into two groups:thirty patients in group A were treated with cilostazol and telmisartan based on routine treatment, while thirty patients in group B were treated with telmisartan a-lone. The levels of 24-h urinary albumin, blood pressure, MCP-1, sICAM-1, alanine aminotransferase, creatinine and glycosy-lated hemoglobin in two groups were compared before treatment and 4 weeks after treatment. Results The levels of 24-h urinary albumin, MCP-1 and sICAM-1 were significantly decreased in both groups after treatment for four weeks, and the differences were significant (P<0. 05). After treatment, the levels of 24-h urinary albumin, MCP-1 and sICAM-1 in group A were obvious-ly lower than those in group B (P<0. 05). Conclusion Cilostazol combined with telmisartan can significantly decrease the uri-nary albumin level in the patients with early type 2 diabetes nephropathy, it can protect the kidney, and delay the progression of early diabetic nephropathy. It is relatively safe in clinical application.%目的:观察西洛他唑联合替米沙坦对早期2型糖尿病肾病( diabetic nephropathy, DN)血清单核细胞趋化蛋白1(MCP-1)和可溶性细胞间黏附分子1(sICAM-1)的影响。方法将我院收治的早期2型DN 60例随机分为西洛他唑联合替米沙坦组和替米沙坦组两组各30例,在常规治疗基础上西洛他唑联合替米沙坦组予西洛他唑和替米沙坦治疗,替米沙坦组仅予替米沙坦治疗,观察比较两组治疗前及治疗4周后24 h尿微量白蛋白、血压及血清MCP-1、sIcAM-1、丙氨酸转氨酶、肌酐、糖化血红蛋白水平。结果治疗4周后,两组24 h尿微量白蛋白及血清MCP-1、sIcAM-1均较

  9. Cell surface adhesion molecules and cytokine profiles in primary progressive multiple sclerosis

    DEFF Research Database (Denmark)

    Ukkonen, Maritta; Wu, Xingchen; Reipert, Birgit;

    2007-01-01

    OBJECTIVE: We evaluated the utility of adhesion molecule (AM) and cytokine/chemokine expressions in blood and cerebrospinal fluid (CSF) as markers of disease activity in primary progressive multiple sclerosis (PPMS). METHODS: The expressions of AMs and the levels of 17 cytokines in patients......) and intercellular adhesion molecule 1 (ICAM-1) in blood and CSF were higher in PPMS than in controls. Comparison between PPMS and SPMS showed higher levels of ICAM-1 in blood and CSF in PPMS, while the level of the vascular adhesion molecule (VCAM-1) was higher only in blood. There was no difference in the levels...... of cytokines in serum or CSF between PPMS and SPMS or controls, but evidence suggesting intrathecal synthesis of interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) was found in PPMS. The expressions of CSF VLA-4 in PPMS correlated with the total volume of cerebral lesions and the number...

  10. CXC chemokine ligand 12/Stromal cell-derived factor-1 regulates cell adhesion in human colon cancer cells by induction of intercellular adhesion molecule-1

    OpenAIRE

    Tung Shui-Yi; Chang Shun-Fu; Chou Ming-Hui; Huang Wen-Shih; Hsieh Yung-Yu; Shen Chien-Heng; Kuo Hsing-Chun; Chen Cheng-Nan

    2012-01-01

    Abstract Background The CXC chemokine ligand 12 (CXCL12)/stromal cell-derived factor-1 (SDF-1) and CXC receptor 4 (CXCR4) axis is involved in human colorectal cancer (CRC) carcinogenesis and can promote the progression of CRC. Interaction between CRC cells and endothelium is a key event in tumor progression. The aim of this study was to investigate the effect of SDF-1 on the adhesion of CRC cells. Methods Human CRC DLD-1 cells were used to study the effect of SDF-1 on intercellular adhesion m...

  11. An analysis of the binding characteristics of a panel of recently selected ICAM-1 binding Plasmodium falciparum patient isolates

    DEFF Research Database (Denmark)

    Madkhali, Aymen M; Alkurbi, Mohammed O; Szestak, Tadge;

    2014-01-01

    EMP1) expressed on the surface of the infected erythrocyte membrane. One of the commonly used host receptors is ICAM-1, and it has been suggested that ICAM-1 has a role in cerebral malaria pathology, although the evidence to support this is not conclusive. The current study examined the cytoadherence...... patterns of lab-adapted patient isolates after selecting on ICAM-1. We investigated the binding phenotypes using variant ICAM-1 proteins including ICAM-1Ref, ICAM-1Kilifi, ICAM-1S22/A, ICAM-1L42/A and ICAM-1L44/A using static assays. The study also examined ICAM-1 blocking by four anti-ICAM-1 monoclonal...... previous observations that this variation might be due to variable contact residues on ICAM-1 being used by different parasite PfEMP1 variants....

  12. CD54/intercellular adhesion molecule 1 and major histocompatibility complex II signaling induces B cells to express interleukin 2 receptors and complements help provided through CD40 ligation

    DEFF Research Database (Denmark)

    Poudrier, J; Owens, T

    1994-01-01

    We have examined signaling roles for CD54 intercellular adhesion molecule 1 and major histocompatibility complex (MHC) II as contact ligands during T help for B cell activation. We used a T helper 1 (Th1)-dependent helper system that was previously shown to be contact as well as interleukin 2 (IL-2......) dependent to demonstrate the relative roles of CD54, MHC II, and CD40 signaling in the events leading to the induction of B cell proliferation and responsiveness to IL-2. Paraformaldehyde-fixed activated Th1-induced expression of IL-2R alpha, IL-2R beta, and B7, and upregulated MHC II and CD54 on B cells...

  13. Amino acid sequences mediating vascular cell adhesion molecule 1 binding to integrin alpha 4: homologous DSP sequence found for JC polyoma VP1 coat protein

    Directory of Open Access Journals (Sweden)

    Michael Andrew Meyer

    2013-07-01

    Full Text Available The JC polyoma viral coat protein VP1 was analyzed for amino acid sequences homologies to the IDSP sequence which mediates binding of VLA-4 (integrin alpha 4 to vascular cell adhesion molecule 1. Although the full sequence was not found, a DSP sequence was located near the critical arginine residue linked to infectivity of the virus and binding to sialic acid containing molecules such as integrins (3. For the JC polyoma virus, a DSP sequence was found at residues 70, 71 and 72 with homology also noted for the mouse polyoma virus and SV40 virus. Three dimensional modeling of the VP1 molecule suggests that the DSP loop has an accessible site for interaction from the external side of the assembled viral capsid pentamer.

  14. Molecular Mechanisms of Curcumin on Diabetes-Induced Endothelial Dysfunctions: Txnip, ICAM-1, and NOX2 Expressions

    Directory of Open Access Journals (Sweden)

    Natchaya Wongeakin

    2014-01-01

    Full Text Available We aim to investigate the effects of curcumin on preventing diabetes-induced vascular inflammation in association with its actions on Txnip, ICAM-1, and NOX2 enzyme expressions. Male Wistar rats were divided into four groups: control (CON, diabetic (DM; streptozotocin (STZ, i.v. 55 mg/kg BW, control-treated with curcumin (CONCUR; 300 mg/kg BW, and diabetes treated with curcumin (DMCUR; 300 mg/kg BW. 12th week after STZ injection, iris blood perfusion, leukocyte adhesion, Txnip, p47phox, and malondialdehyde (MDA levels were determined by using laser Doppler, intravital fluorescent confocal microscopy, Western Blot analysis, and TBAR assay, respectively. The iris blood perfusion of DM and DMCUR was decreased significantly compared to CON and CONCUR (P<0.001. Plasma glucose and HbA1c of DM and DMCUR were increased significantly compared to CON and CONCUR (P<0.001. Leukocyte adhesion, ICAM-1, p47phox expression, and MDA levels in DM were increased significantly compared to CON, CONCUR, and DMCUR (P<0.05. Txnip expression in DM and DMCUR was significantly higher than CON and CONCUR (P<0.05. From Pearson’s analysis, the correlation between the plasma MDA level and the endothelial functions was significant. It suggested that curcumin could ameliorate diabetic vascular inflammation by decreasing ROS overproduction, reducing leukocyte-endothelium interaction, and inhibiting ICAM-1 and NOX2 expression.

  15. Different effects of antisense RelA p65 and NF-κB1 p50 oligonucleotides on the nuclear factor-κB mediated expression of ICAM-1 in human coronary endothelial and smooth muscle cells

    Directory of Open Access Journals (Sweden)

    Both Anton

    2001-08-01

    Full Text Available Abstract Background Activation of nuclear factor-κB (NF-κB is one of the key events in early atherosclerosis and restenosis. We hypothesized that tumor necrosis factor-α (TNF-α induced and NF-κB mediated expression of intercellular adhesion molecule-1 (ICAM-1 can be inhibited by antisense RelA p65 and NF-κB1 p50 oligonucleotides (RelA p65 and NF-κB1 p50. Results Smooth muscle cells (SMC from human coronary plaque material (HCPSMC, plaque material of 52 patients, SMC from the human coronary media (HCMSMC, human endothelial cells (EC from umbilical veins (HUVEC, and human coronary EC (HCAEC were successfully isolated (HCPSMC, HUVEC, identified and cultured (HCPSMC, HCMSMC, HUVEC, HCAEC. 12 hrs prior to TNF-α stimulus (20 ng/mL, 6 hrs RelA p65 and NF-κB1 p50 (1, 2, 4, 10, 20, and 30 μM and controls were added for a period of 18 hrs. In HUVEC and HCAEC there was a dose dependent inhibition of ICAM-1 expression after adding of both RelA p65 and NF-κB1 p50. No inhibitory effect was seen after incubation of HCMSMC with RelA p65 and NF-κB1 p50. A moderate inhibition of ICAM-1 expression was found after simultaneous addition of RelA p65 and NF-κB1 p50 to HCPSMC, no inhibitory effect was detected after individual addition of RelA p65 and NF-κB1 p50. Conclusions The data point out that differences exist in the NF-κB mediated expression of ICAM-1 between EC and SMC. Experimental antisense strategies directed against RelA p65 and NF-κB1 p50 in early atherosclerosis and restenosis are promising in HCAEC but will be confronted with redundant pathways in HCMSMC and HCPSMC.

  16. ICAM-1 triggers liver regeneration through leukocyte recruitment and Kupffer cell-dependent release of TNF-alpha/IL-6 in mice.

    NARCIS (Netherlands)

    Selzner, N; Selzner, M; Odermatt, B; Tian, Y; Rooijen, van N.; Clavien, PA

    2003-01-01

    AIMS: Tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 mediate hepatocyte proliferation in vivo, suggesting that local and systemic inflammatory reactions may trigger hepatic regeneration after major tissue loss. METHODS: Wild-type, intercellular adhesion molecule (ICAM)-1-/-, and neutropeni

  17. Effect of non-surgical periodontal therapy on level of serum soluble intercellular adhesion molecule-1 and glycated hemoglobin A1c in patients with type 2 diabetes and chronic periodontitis%牙周非手术治疗对2型糖尿病伴牙周炎患者糖化血红蛋白A1c和血清可溶性细胞间黏附分子-1的影响

    Institute of Scientific and Technical Information of China (English)

    袁堂霞; 张彦表; 周云; 王凡涛; 王峰

    2013-01-01

    Objective To evaluate the effects of non-surgical periodontal treatment on clinical periodontal measurements,glycemic control,and level of serum soluble intercellular adhesion molecule-1 (sICAM-1) in type 2 diabetes mellitus with chronic periodontitis patients.Methods Patients with type 2 diabetes and chronic periodontitis were selected and classified into well-controlled group[glycated hemoglobin A1c(GHbA1c)<7.00%,n=30,DMCP1 group] and poorly-controlled group (GHbA1c≥ 7.00%,n=30,DMCP2 group).Thirty systemically healthy patients with chronic periodontitis were recruited as control group (CP group),All subjects underwent non-surgical periodontal therapy.Plaque index(PLI),sulcus bleeding index (SBI),bleeding on probing(BOP),probing depth (PD),clinical attachment loss (CAL),serum sICAM-1 concentration,and the value of fasting plasma glucose(FPG),GHbA1c were recorded at baseline,1 and 3 months after periodontal treatment.Results The three study groups showed significant improvements for the levels of PD,SBI,PLI,BOP,and serum sICAM-1 concentration at 1 and 3 months after non-surgical periodontal treatment (P<0.05).The level of CP group and DMCP1 group also showed significant improvements for the levels of CAL(P<0.05),but no significant change was found in DMCP2 group(P>0.05).At 3 months after periodontal treatment,GHbA1c levels in DMCP2 group significantly decreased by 1.12%(P<0.05),whereas no significant changes were found in CP and DMCP1 groups (P>0.05).Conclusion Non-surgical periodontal treatment can significantly improve periodontal health status in patients with type 2 diabetes and periodontitis,reduce the level of serum sICAM-1,and can reduce the level of GHbA1c in poorly controlled type 2 diabetic patients.%目的 探讨牙周非手术治疗对2型糖尿病伴慢性牙周炎(DMCP)患者牙周状况、糖代谢及血清可溶性细胞间黏附分子-1 (sICAM-1)的影响.方法 选择诊断为2型糖尿病伴慢性牙周炎的

  18. 三伏灸对支气管哮喘患者血浆sICAM-1、sVCAM-1和sE-slectin水平的影响%Effect of Dog Day Moxibustion on Soluble Cellular Adhesion Molecules in Treating Bronchial Asthma

    Institute of Scientific and Technical Information of China (English)

    杨君军; 唐纯志; 赖新生

    2005-01-01

    目的:观察三伏灸对支气管哮喘患者血浆可溶性细胞黏附分子的影响,探讨三伏灸治疗支气管哮喘作用机制.方法:对28例哮喘缓解期患者行三伏灸治疗,观察3个月后的近期疗效,于治疗前及治疗后10 d分别检测血浆可溶性细胞黏附分子(sCAM)及IgE水平,并与10例正常人作对照.结果:三伏灸治疗支气管哮喘的总有效率为92.86%.三伏灸能显著降低患者血浆可溶性细胞间黏附分子-1(sICAM-1)水平和血清IgE含量(P﹤0.01),降低血浆可溶性血管-细胞间黏附分子-1(sVCAM-1)和可溶性E选择素(sE-selectin)水平(P﹤0.05).患者血清IgE含量与sICAM-1含量呈显著相关性(r =0.641,P =0.000),sICAM-1与sVCAM-1之间亦呈正相关(r =0.449,P=0.017).结论:三伏灸可能通过抑制黏附分子的表达或直接抑制白细胞与内皮细胞的黏附,从而减少炎细胞的浸润,达到治疗效果.

  19. Comparative Study of Serum Soluble Intercellular Adhesion Molecule-1 in Different Obese Women with Polycystic Ovary Syndrome%不同肥胖标准PCOS患者血清可溶性细胞间黏附分子-1水平比较

    Institute of Scientific and Technical Information of China (English)

    黄卡立; 蒋凤艳; 胡芸

    2011-01-01

    目的:比较不同肥胖标准的多囊卵巢综合征(PCOS)患者血清可溶性细胞间黏附分子-1(sICAM-1)水平差异.方法:将PCOS患者以体质量指数(BMI)≥24 ks/m2为肥胖标准分为肥胖A组和非肥胖A组,以腰臀比(WHR)≥0.8为肥胖标准,分为肥胖B组和非肥胖B组,以BMI≥24 kg/m2且WHR≥0.8为肥胖标准分为肥胖C组和非肥胖C组,比较不同组别间的血清sICAM-1水平,并分析sICAM-1水平与BMI、WHR的相关性.结果:肥胖A、B、C组血清sICAM-1水平较对应的非肥胖A、B、C组显著升高(P0.05);非肥胖A组患者血清sICAM-1水平高于非肥胖B组、C组患者(均P0.05);血清sICAM-1水平与BMI、WHR均呈正相关(r分别为0.204和0.360,均P<0.05).结论:PCOS患者血清aICAM-1水平与肥胖有密切联系,PCOS患者sICAM-1水平随着WHR及BMI增大而升高.%Objective:To study the level of serum soluble intercellular adhesion molectle-1 (sICAM-1) in obese women with polycystic ovary syndrome (PCOS). Methods: The obese patients with PCOS were divided into two goups (obese A group and non-obese A group) according to the standard of body mass index (BMI) ≥ 24 kg/m2. The patients were divided into two goups (obese B group and non-obese B group) according to the standard of waist-hip ratio (WHR) ≥ 0.8. The patients were also divided into two groups(obese C groups and non-obese C group) according to the standard of BMI ≥ 24 kg/m2 and WHR≥ 0.8. The serum levels of sICAM-1 were compared between groups. The correlation was analysed between the level of sICAM-1 and the values of BMI and WHR. Results :The serum levels of sICAM-1 were significantly higher in obese A, obese B and obese C groups than those of non-obese A, non-obese B and non-obese C groups (P< 0.05). There were no signficant differences in serum levels of sICAM-1 between obese A, obese B and obese C groups (P > 0.05).The serum level of sICAM-1 was significant higher in non-obese A group than that of non-obese B group and non

  20. Evidence for elevated (LIMK2 and CFL1) and suppressed (ICAM1, EZR, MAP2K2, and NOS3) gene expressions in metabolic syndrome.

    Science.gov (United States)

    Tabur, Suzan; Oztuzcu, Serdar; Oguz, Elif; Demiryürek, Seniz; Dagli, Hasan; Alasehirli, Belgin; Ozkaya, Mesut; Demiryürek, Abdullah T

    2016-08-01

    The metabolic syndrome (MetS) is a common multicomponent condition including abdominal obesity, dyslipidemia, hypertension, and hyperglycaemia. The aim of this study was to investigate the associations of the expression of a panel of signalling genes with the MetS in a Turkish population. A total of 54 MetS patients and 42 healthy controls with similar age and sex were included to this study. mRNA from blood samples was extracted, and real-time polymerase chain reaction was performed for gene expressions using a BioMark 96.96 dynamic array system. We observed marked increases in LIM kinase 2 (LIMK2) and cofilin 1 (CFL1) gene expressions in MetS patients. However, there were significant decreases in intercellular adhesion molecules 1 (ICAM1), ezrin (EZR), mitogen-activated protein kinase kinase 2 (MAP2K2), and nitric oxide synthase 3 (NOS3) gene expressions in MetS patients. Additionally, no marked changes were noted in other 15 genes studied. This is the first study to provide evidence that activation of LIMK2/CFL1 pathway may play an important role in MetS. PMID:26956845

  1. 奇智方对人脐静脉内皮细胞ICAM-1ICAM-1mRNA 表达的影响

    Institute of Scientific and Technical Information of China (English)

    张淑霞

    2010-01-01

    目的 采用人脐静脉内皮细胞(HUVEC-304)进行细胞间黏附分子-1(ICAM-1)及其转录水平(ICAM-1mRNA)表达的离体实验研究,观察奇智方对血管内皮功能的作用.方法 应用ELISA方法检测ICAM-1;用原位杂交的方法检测ICAM-1mRNA.结果 中药治疗组和阳性对照组与生理盐水组比较,ICAM-1蛋白分子表达均有统计学意义(P<0.01);中药治疗组和阳性对照组均能明显使缺氧/复氧后细胞ICAM-1mRNA下调,与缺氧组比较有统计学意义(P<0.01).结论 奇智方抑制缺氧/复氧后血管内皮细胞表达ICAM-1ICAM-1mRNA,从而保护血管内皮细胞的屏障完整和功能正常,可能是其免疫抑制机理的分子基础之一.

  2. The preparation of cells (A549) with measurement of the relative downstream differential expression of ICAM-1

    Science.gov (United States)

    Eleghasim, Ndukauba M.; Haddrell, Allen E.; van Eeden, Stephen; Agnes, George R.

    2006-12-01

    The characterization of particulate matter suspended in the troposphere (PM10) based on size is an important basis for assessing the extent of their adverse effects on human health. The relevance of such assessments is anticipated to be significantly improved through the continued development of tools that can identify the chemical components within individual ambient particles, and the injury that they cause. We use recently reported methodology to create mimics of ambient particle types of known size and chemical composition that are levitated within an ac trap. The ac trap uses electric fields to levitate the particles that have a given mass and net elementary charge, and as such the ac trap is a mass-to-charge filter. The ac trap was used to levitate populations of particles where the size of particles in any given population could be altered. The levitated particles are delivered direct from the ac trap to human lung cells (A549), in vitro, with downstream measurement of differential expression of intercellular adhesion molecule (ICAM)-1 and counting of the number of particles actually delivered to the culture using an optical microscope. In this study, the chemical composition of the ambient particle mimics was restricted to inorganic compounds whose relative abundance was purposely designed to mimic the average abundance in Environmental Health Center-93 (EHC-93) particles. The sizes of the multilelement particle types prepared were 6.8 +/- 0.5, 3.8 +/- 0.3, 2.6 +/- 0.2 (mean +/- S.D.). Particles of either elemental carbon, or elemental carbon containing glycerol were used as control particle types. In any given experiment, a known number of particles, but always cell culture. Following an 18-h incubation period and anti-body labeling of ICAM-1, the fluorescence emission from a 1.07 mm2 area of the cell culture centered at the site of particle deposition was acquired. The relative differential expression of ICAM-1 was greatest for multielement particle types

  3. Inhibition of ICAM-1 expression in renal tubular epithelial cells with ICAM-1 antisense oligodeoxynucleotide%ICAM-1反义寡核苷酸对小鼠肾小管上皮细胞ICAM-1表达的影响

    Institute of Scientific and Technical Information of China (English)

    程庆砾; 陈香美; 傅博; 叶一舟

    2000-01-01

    目的:探讨ICAM-1反义寡核苷酸对小鼠肾小管上皮细胞表达ICAM-1的影响,为利用ICAM-1反义寡核苷酸类药物治疗肾小管间质病变奠定基础.方法:小鼠ICAM-1反义寡核苷酸及其对照物参照文献合成并行全硫代磷酸化修饰.部分ICAM-1反义寡核苷酸在其5'端作FITC荧光标记.将ICAM-1反义寡核苷酸单独或脂质体转染试剂DOTAP混合后转染至培养的肾小管上皮细胞之中,转染成功后加入IL-1β诱导细胞产生ICAM-1.采用对照寡核苷酸及不含寡核苷酸的细胞转染液作为实验对照及空白对照.利用免疫组化染色的方法检测细胞ICAM-1表达变化并提取细胞总RNA行逆转录PCR及Northern杂交观察ICAM-1 mRNA的表达的变化.结果:两个不同浓度的ICAM-1反义寡核苷酸均可明显阻断IL-1β诱导的肾小管上皮细胞ICAM-1ICAM-1 mRNA的表达;对照的寡核苷酸不能减少IL-1β诱导的肾小管上皮细胞ICAM-1ICAM-1 mRNA的表达.结论:小鼠ICAM-1反义寡核苷酸可明显抑制IL-1β诱导的小鼠肾小管上皮细胞ICAM-1ICAM-1 mRNA 的表达,提示ICAM-1的反义寡核苷酸有可能应用于肾小管间质病变的实验治疗之中.

  4. The Expression of Human Intercellular Adhesion Molecule-1 in Eukaryotic Cell and the Identification of their Products%人细胞间黏附分子-1的真核细胞表达与鉴定

    Institute of Scientific and Technical Information of China (English)

    陈志鸿; 静雅杰; 宋宝辉; 梁军

    2008-01-01

    Objective To construct ICAM-1 eukaryotie expression vectors and to express them in COS7 cells.Methods ICAM-1 cDNA was amplified by PCR and then inserted into the pcDNA 3.1(-)vector to construct recombinant vectors,and were transfected into COS-7 cells under the mediation of liposome.The expressed ICAM-1 fusion protein was detected by Western blot.The expression of ICAM-1 fusion protein Was observed under fluorescence microscope.Results 1800 bp ICAM-1 cDNA Was obtained by PCR.The PCR product was successfully ligated with pcDNA 3.1(-)vector.Restriction endonuclease digestion analysis and DNA sequencing showed that recombinant pcDNA 3.1(-)-ICAM-1 was successfully constructed.Conclusion Eukaryotie expression recombinant vector pcDNA 3.1(-)-ICAM-1 is constructed and expressed successfully,which lays the foundation for the functional research of ICAM-1 and for the preparation of mAb to ICAM-1.%目的 构建人细胞间黏附分子-1(ICAM-1)真核表达载体PcDNA3.1(-)-ICAM-1,并在真核细胞COS-7中表达.方法 设计特异性引物,用PCR方法扩增ICAM-1全编码区基因片段,将其连接人真核表达载体pcDNA3.1(-),并通过酶切进行鉴定.用脂质体转染法将真核表达载体pcDNA3.1(-)-ICAM-1转染COS-7细胞,通过免疫荧光和Western印迹分析人ICAM-1蛋白在COS-7细胞中的表达情况.结果 PCR扩增得到人ICAM-1的cDNA片段大小为1800 bp,重组质粒经酶切鉴定和DNA序列分析确定得到真核表达载体peDNA3.1(-)-ICAM-1.荧光显微镜下可见转染重组质粒的COS-7细胞膜上存在荧光分布,而转染空质粒的细胞未见荧光分布.Western印迹检测发现转染重组质粒的细胞存在外源性的人ICAM-1表达,而转染空质粒的则未见ICAM-1表达.结论 成功构建了人ICAM-1真核表达载体,ICAM-1高效表达在转染的真核细胞COS-7表面,为进一步建立稳定表达ICAM-1的COS-7细胞株以及研究ICAM-1及其受体的生物学功能提供了条件.

  5. Cryptotanshinone inhibits oxidized LDL-induced adhesion molecule expression via ROS dependent NF-κB pathways.

    Science.gov (United States)

    Zhao, Wenwen; Wu, Chuanhong; Chen, Xiuping

    2016-05-01

    Adhesion molecules, such as intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin, play important roles in the initial stage of atherosclerosis. Cryptotanshinone (CPT), a natural compound isolated from Salvia miltiorrhiza Bunge, exhibits anti-atherosclerotic activity although the underlying mechanisms remain elusive. In this study, the protective effect of CPT against oxidized low-density lipoprotein (ox-LDL)-induced adhesion molecule expression was investigated in human umbilical vein endothelial cells. Ox-LDL significantly induced ICAM-1, VCAM-1, and E-selectin expression at the mRNA and protein levels but reduced eNOS phosphorylation and NO generation, which were reversed by CPT pretreatment. Sodium nitroprusside, a NO donor, N-acetyl-L-cysteine (NAC), a reactive oxygen species (ROS) scavenger, and BAY117082, a NF-κB inhibitor, inhibited ox-LDL-induced ICAM-1, VCAM-1, and E-selectin expression. Ox-LDL-induced ROS production was significantly inhibited by CPT and NAC. Furthermore, ox-LDL activated the NF-κB signaling pathway by inducing phosphorylation of IKKβ and IκBα, promoting the interaction of IKKβ and IκBα, and increasing p65 nuclear translocation, which were significantly inhibited by CPT. In addition, CPT, NAC, and BAY117082 inhibited ox-LDL-induced membrane expression of ICAM-1, VCAM-1, E-selectin, and endothelial-monocyte adhesion and restored eNOS phosphorylation and NO generation. Results suggested that CPT inhibited ox-LDL-induced adhesion molecule expression by decreasing ROS and inhibiting the NF-κB pathways, which provides new insight into the anti-atherosclerotic mechanism of CPT. PMID:26647279

  6. Circulating CD133+CD34+ progenitor cells inversely correlate with soluble ICAM-1 in early ischemic stroke patients

    Directory of Open Access Journals (Sweden)

    Frank Joseph

    2011-08-01

    Full Text Available Abstract Background and Purpose Both endothelial progenitor cells (EPC and markers of neuroinflammation are candidate biomarkers for stroke severity and outcome prediction. A relationship between EPC and neuroinflammatory markers in early stroke is not fully elucidated. The objectives were to investigate correlations between EPC and neuroinflammation markers (adhesion molecules ICAM-1, VCAM-1, E-selectin, tumor necrosis factor (TNF-α, interleukin (IL-6, endothelin (ET-1, markers of tissue injury (matrix metalloproteinases (MMP-9 and tissue inhibitor of matrix metalloproteinases (TIMP-1 in early stroke patients. Methods We prospectively recruited symptomatic patients with ischemic cerebrovascular disease. We assessed stroke severity by using of acute (diffusion-weighted imaging (DWI and final lesion volumes (fluid attenuated inversion recovery (FLAIR. We measured serum soluble ICAM-1, VCAM-1, E-selectin, MMP-9, TIMP-1 and plasma TNF-α, IL-6, ET-1 by ELISA, and quantified EPC in mononuclear fraction of peripheral blood on days 1 and 3 in 17 patients (mean(SD age 62(14, with admission National Institutes of Health Stroke Scale (NIHSS 10(8 selected from 175 patients with imaging confirmed ischemic stroke. Non-parametric statistics, univariate and multivariate analysis were used. Results Only ICAM-1 inversely correlated with EPC subset CD133+CD34+ on day 1 (Spearman r = -0.6, p Conclusion Our study showed that high ICAM-1 is associated with low CD133+CD34+subset of EPC. Biomarkers of neuroinflammation may predict tissue injury and stroke severity in early ischemia.

  7. Activation of AMP-activated protein kinase attenuates hepatocellular carcinoma cell adhesion stimulated by adipokine resistin

    International Nuclear Information System (INIS)

    Resistin, adipocyte-secreting adipokine, may play critical role in modulating cancer pathogenesis. The aim of this study was to investigate the effects of resistin on HCC adhesion to the endothelium, and the mechanism underlying these resistin effects. Human SK-Hep1 cells were used to study the effect of resistin on intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expressions as well as NF-κB activation, and hence cell adhesion to human umbilical vein endothelial cells (HUVECs). 5-Aminoimidazole-4-carboxamide 1-β-D-ribofuranoside (AICAR), an AMP-activated protein kinase (AMPK) activator, was used to determine the regulatory role of AMPK on HCC adhesion to the endothelium in regard to the resistin effects. Treatment with resistin increased the adhesion of SK-Hep1 cells to HUVECs and concomitantly induced NF-κB activation, as well as ICAM-1 and VCAM-1 expressions in SK-Hep1 cells. Using specific blocking antibodies and siRNAs, we found that resistin-induced SK-Hep1 cell adhesion to HUVECs was through NF-κB-regulated ICAM-1 and VCAM-1 expressions. Moreover, treatment with AICAR demonstrated that AMPK activation in SK-Hep1 cells significantly attenuates the resistin effect on SK-Hep1 cell adhesion to HUVECs. These results clarify the role of resistin in inducing HCC adhesion to the endothelium and demonstrate the inhibitory effect of AMPK activation under the resistin stimulation. Our findings provide a notion that resistin play an important role to promote HCC metastasis and implicate AMPK may be a therapeutic target to against HCC metastasis

  8. Synthesis and Identification of ICAM-1 Mimicry Peptide%ICAM-1表位模拟肽的合成与鉴定

    Institute of Scientific and Technical Information of China (English)

    郝文波; 徐伟文; 李明; 王萍

    2005-01-01

    目的对合成的 ICAM- 1模拟肽 P1(KLYLIAEGSVAA) 的抗原性及生物活性进行鉴定. 方法化学合成 ICAM- 1模拟肽 KLYLIAEGSVAA,以间接 ELISA及竞争抑制试验鉴定合成肽的抗原性,以玻片免疫组化方法鉴定合成肽的生物活性.结果合成肽能与抗 ICAM- 1单抗 15.2发生特异性结合,并且能够竞争抑制 ICAM- 1分子及相应的阳性噬菌体克隆与单抗 15.2的结合作用.玻片免疫组化显示合成肽及 ICAM- 1分子均能有效抑制相应的阳性噬菌体展示肽与白细胞的结合.结论合成的短肽具有 ICAM- 1与 15.2抗体结合的抗原性,并能有效模拟 ICAM- 1分子与白细胞结合的功能.

  9. Increased ICAM-1 expression on epithelial cells induced by TNF-α%TNF-α诱导支气管上皮细胞表达ICAM-1

    Institute of Scientific and Technical Information of China (English)

    王成彬; 黄振国; 叶伟基; 田亚平; 林伟基

    2005-01-01

    目的:探讨支气管上皮细胞活化对ICAM-1基因和细胞表面ICAM-1蛋白质表达的影响.方法:用10ng/ml TNF-α作用于正常培养的支气管上皮细胞(BEAS-2B) 12h,通过RT-PCR分析ICAM-1在BEAS-2B细胞中的基因表达和用流式细胞仪分析ICAM-1在BEAS-2B细胞表面蛋白质量.结果:TNF-α与BEAS-2B细胞共同培养12h,可上调BEAS-2B细胞ICAM-1基因的表达和增加BEAS-2B细胞表面的ICAM-1蛋白质量.结论:TNF-α可诱导BEAS-2B 细胞ICAM-1基因和蛋白质表达.

  10. Effects of Triptolide on Expression of AIF and ICAM-1 in Rat's Kidney Tissure with Renal Ischemia Reperfusion Injury%雷公藤内酯醇对肾缺血再灌注大鼠凋亡诱导因子及细胞间黏附分子-1表达的影响

    Institute of Scientific and Technical Information of China (English)

    包自阳; 朱彩凤; 李苞芳; 朱斌; 汤绚丽

    2012-01-01

    目的:探讨雷公藤内酯醇(TP)对肾缺血再灌注(I/R)大鼠的肾保护作用,及对凋亡诱导因子、细胞间黏附分子-1的影响.方法:48只雄性Wistar大鼠随机分为假手术组、I/R模型组(I/R组)、TP高、中、低剂量干预组、泼尼松对照组(Pred组).采用夹闭双侧肾动脉30 min,再灌注18 h的方法制作肾I/R大鼠模型.检测血肌酐(Scr)、尿素氮(BUN),原位末端标记法检测肾小管上皮细胞凋亡,观察肾病理改变,计算肾小管损伤(ATN)评分.Western印迹和RT-PCR分别检测AIF、ICAM-1蛋白和基因表达.结果:(1)I/R组血Scr、BUN、ATN评分及细胞凋亡指数较假手术组显著升高(P<0.01);与I/R组比较,TP各组以上指标均改善(P<0.01),pred组血Scr、BUN、ATN评分改善(P<0.01),但细胞凋亡指数无明显变化(P>0.05).(2)I/R组大鼠肾组织AIF、ICAM-1较假手术组高表达(P<0.01);与I/R组比较,TP各组二者表达均减弱(P<0.01),pred组ICAM-1表达减弱(P<0.01)但AIF表达差异无统计学意义(P>0.05).结论:TP对肾I/R大鼠具有肾保护作用,其部分机制可能与抑制肾小管上皮细胞过度凋亡及AIF、ICAM-1表达有关.%Objective: To explore protective effect of Triptolide ( TP ) on rat' s kidney from renal ischemia reperfusion ( 1/ R ) injury and interference effect on expression level of apoptosis - inducing factor ( AIF ) and intercellular adhesion molecule - 1 and ( ICAM - 1 ). Methods:48 male Wistar rats were randomly divided into six groups: sham operation group, ischemia reperfusion injury group ( I/R group ), low TP group, medium TP group, high TP group, prednisone group ( Pred group ). The renal I/R rat model was duplicated by clamping Bilateral renal artery for 30 minutes and then artery reperfusion for 18 hours. The levels of serum creatinine ( Scr ) and Blood urea nitrogen ( Bun ) were detected. Apoptosis of tubular epithelial cell was determined by terminal deoxynucleotidy transferase dUTP nick end labeling

  11. Effect of exendin-4 on the expression of NF-κB p65 and ICAM-1 in aorta endothelium of type 2 diabetic rats%Exendin-4对2型糖尿病大鼠主动脉内皮核因子-κB和细胞间黏附分子-1表达的影响

    Institute of Scientific and Technical Information of China (English)

    李伟; 李培培; 李秀琴; 范爱红

    2009-01-01

    目的 探讨Exendin-4对2型糖尿病大鼠主动脉内皮NF-κB p65以及细胞间黏附分子-1(ICAM-1)表达的影响.方法 选择40只雄性SD大鼠,6只喂基础饲料为正常对照组(NC组),另34只喂高脂饲料4周后,一次性腹腔注射链脲佐菌素,建立2型糖尿病大鼠模型,维持2周,24只大鼠造模成功,并分为糖尿病组(DM组)、Exendin-4低剂量治疗组(GL组)、中剂量治疗组(GM组)、高剂量治疗组(GH组),每组6只,给予不同剂量Exendin-4腹腔注射治疗6周.心脏采血检测丙二醛(MDA)、超氧化物歧化酶(SOD)、总抗氧化能力(T-AOC)水平.之后分离胸主动脉,免疫组织化学方法现察主动脉内皮NF-κB p65和ICAM-1的表达.结果 与NC组比较,DM组MDA升高.SOD和T-AOC降低(P<0.05).与DM组比较,GH组MDA降低,SOD、T-AOC升高;且NF-κB p65表达明显降低(P<0.05).与GL组比较,GM组、GH组ICAM-1表达明显降低,差异均有统计学意义(P<0.05).结论 Exendin-4具有血管内皮保护作用,其机制与抗氧化、抑制血管内皮NF-κB p65、ICAM-1的活化有关.%Objective To explore the influence of exendin-4 on antioxidation index in serum and the expression of nuclear factor Kappa B (NF-κB)p65 and intercellular cell adhesion molecule-1(ICAM-1) in aorta endothelium of type 2 diabetic rats and the possible mechanism. Methods The normal rats were injected with streptozocin(STZ) into abdominal cavity after high fat diet to es-tablish the model of type 2 diabetic rats. Forty SD male rats were randomly divided into normal control group,diabetic model group and groups treated with low, medium, and high dose of ex-endin-4. The treated groups were treated with intraperitoneal injection of exendin-4 for six weeks.Heart blood was taken for examining biochemical indexes including malondialdehyde(MDA), SOD and total antioxidation capability(T-AOC). The thoracic aorta was isolated carefully to observe the expression of NF-κB p65 and ICAM-1 in endothelium with

  12. Relationship between the different immune status of HBV infection and the expression of sICAM-1%HBV感染不同免疫状态患者血清中可溶性细胞间粘附分子-1水平的变化

    Institute of Scientific and Technical Information of China (English)

    杨丽莎; 罗伟生; 覃理灵; 何武; 周劲刚; 王钊; 吴淋玲; 黄亚琴

    2011-01-01

    目的:探讨可溶性细胞间粘附分子-1(sICAM- 1)在乙型肝炎病毒( HBV)感染不同免疫状态及HBV感染相关原发性肝癌( PHC)患者血清中的变化及其意义.方法:将HBV感染者及HBV感染相关PHC患者分为5组:HBV感染免疫耐受组80例、免疫清除组80例、免疫不全组80例(其中分免疫不全A组40例、B组40例)和PHC组80例;另选40名非HBV感染健康体检者作为正常对照组,利用ELISA 法对5组者及对照组血清sICAM-1水平进行测定.结果:HBV感染不同免疫状态者中免疫清除、免疫不全B及HBV感染相关PHC患者较正常对照组有不同程度的升高,差别有统计学意义(P<0.05);免疫耐受、免疫不全A组与正常对照组相比差别无统计学意义(P>0.05).结论:血清sICAM-1变化对于判断HBV感染不同免疫状态病情变化,有一定的临床价值.%Objective: To study the expression and significance of the serum levels of soluble intercellular adhesion molecule- 1 (sICAM-1) in patients with different immune status of hepatitis B virus (HBV) infection and Primary Hepatocellular Carcinoma (PHC).Methods: The patients of HBV infection were grouped into five teams,80 cases of immune tolerance to HBV,80 cases of immune clearance, immunodeficiency (A) and immunodeficiency (B) with 40 patients in either groups,and 80 patients diagnosed as PHC clinically.Serum samples were collected from these patients,and from 40 healthy volunteers as control for the study.Serum levels of sICAM-1 were measured by enzyme-linked immunosorbent assay (ELISA).Results:Serum levels of sICAM-1 in patients with immune clearance, immunodeficiency (B) and PHC were significantly increased,comparing with that of normal control ( P < 0.05).Serum levels of sICAM-1 in patients with immune tolerance,immunodeficiency (A) were not significantly different compared with that of normal control ( P > 0.05).Conclusion: Serum levels of sICAM-1 may reflect the disease progressed in patients with

  13. Study on the serum levels of soluble intercellular adhesion molecule—1(slCAM—1) in patients with Helicobacter pylori Infection

    Institute of Scientific and Technical Information of China (English)

    吴勤动; 石益海; 等

    2002-01-01

    Objective:To evaluate the interaction between serum levels of soluble intercellular adhesion molecule-1(sICAM-1) and Helicobacter pylori(H.pylori) infection in patients with chronic gastritis and peptic ulcer.Methods:The serum levels of sICAM-1 in 205 patients with chronic gastric diseases were detected by ELISA method and the status of H.pylori was determined by histologic examination.RUT,14C=UBT,and serology,Ther sera obtained from 18 healthy volunteers served as controls,Results:The serum lervels of sICAM-1 were significantly higher in patients with H.pylori positive than those of H.pylori negative(889.43±32.52ng/mlvs,747.07±30.45ng/ml,P<0.05),The serum levels of sICAM-1 in patients with mild,moderate and severe infection of H.pylori were 841.68±72.36ng/ml,905.43±37.59ng/ml and 1012.54±49.34ng/ml,respectively(P<0.05),The serum levels of sICAM-1 proved to be significantly correlated with the density of H.pylori colonization in gastric mucosa(rs=0.316,P<0.001),The serum levels of sICAM-1 in patients with chronic gastritis and peptic ulcer were significantly higher than those in healthy controls(P<0.05).Conclusions:These results indicated that H.pylori infection up-regulates the expression of sICAM-1.

  14. Ac-SDKP suppresses TNF-α-induced ICAM-1 expression in endothelial cells via inhibition of IκB kinase and NF-κB activation.

    Science.gov (United States)

    Zhu, Liping; Yang, Xiao-Ping; Janic, Branislava; Rhaleb, Nour-Eddine; Harding, Pamela; Nakagawa, Pablo; Peterson, Edward L; Carretero, Oscar A

    2016-05-01

    N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a naturally occurring tetrapeptide that prevents inflammation and fibrosis in hypertension and other cardiovascular diseases. We previously showed that, in angiotensin II-induced hypertension, Ac-SDKP decreased the activation of nuclear transcription factor NF-κB, whereas, in experimental autoimmune myocarditis and hypertension animal models, it also reduced the expression of endothelial leukocyte adhesion molecule ICAM-1. However, the mechanisms by which Ac-SDKP downregulated ICAM-1 expression are still unclear. TNF-α is a proinflammatory cytokine that induces ICAM-1 expression in various cell types via TNF receptor 1 and activation of the classical NF-κB pathway. We hypothesized that in endothelial cells Ac-SDKP suppresses TNF-α-induced ICAM-1 expression by decreasing IKK phosphorylation that as a consequence leads to a decrease of IκB phosphorylation and NF-κB activation. To test this hypothesis, human coronary artery endothelial cells were treated with Ac-SDKP and then stimulated with TNF-α. We found that TNF-α-induced ICAM-1 expression was significantly decreased by Ac-SDKP in a dose-dependent manner. Ac-SDKP also decreased TNF-α-induced NF-κB translocation from cytosol to nucleus, as assessed by electrophoretic mobility shift assay, which correlated with a decrease in IκB phosphorylation. In addition, we found that Ac-SDKP decreased TNF-α-induced IKK phosphorylation and IKK-β expression. However, Ac-SDKP had no effect on TNF-α-induced phosphorylation of p38 MAP kinase or ERK. Thus we conclude that Ac-SDKP inhibition of TNF-α activation of canonical, i.e., IKK-β-dependent, NF-κB pathway and subsequent decrease in ICAM-1 expression is achieved via inhibition of IKK-β.

  15. ICAM-1, VCAM-1, and MAdCAM-1 are expressed on choroid plexus epithelium but not endothelium and mediate binding of lymphocytes in vitro.

    Science.gov (United States)

    Steffen, B J; Breier, G; Butcher, E C; Schulz, M; Engelhardt, B

    1996-06-01

    The expression of cell adhesion molecules (CAMs) in the choroid plexus was studied in normal brain and during experimental autoimmune encephalomyelitis (EAE) in the SJL/J mouse during inflammation induced by intracerebral injection of killed Corynebacterium parvum in the C3H/He mouse. Both ICAM-1 and VCAM-1, but not MAdCAM-1, were constitutively expressed on choroid plexus epithelium but not on the fenestrated capillary endothelial cells within the choroid plexus. During EAE, we observed an up-regulation of ICAM-1 and VCAM-1 and de novo expression of MAdCAM-1 on choroid plexus epithelial cells. In contrast, endothelial cells in the choroid plexus were not induced to express any of the investigated CAMs. In in situ hybridization analysis we demonstrated that ICAM-1, VCAM-1, and MAdCAM-1 were locally synthesized and that the amount of their mRNAs increased in the inflamed choroid plexus. In vitro, primary choroid plexus epithelial cells could be induced to express ICAM-1, VCAM-1, and MAdCAM-1 on their surface after treatment with proinflammatory cytokines such as tumor necrosis factor-alpha, interleukin-1, interferon-gamma, and lipopolysaccharide. To investigate the functional status of the expressed CAMs we performed Stamper-Woodruff binding assays on frozen sections of inflamed and naive brains. ICAM-1, VCAM-1, and MAdCAM-1 expressed in choroid plexus epithelial cells mediated binding of lymphocytes via their known ligands LFA-1 and alpha4-integrin, respectively. The expression of ICAM-1, VCAM-1, and MAdCAM-1 on choroid plexus epithelial cells together with the lack of their expression on the fenestrated choroid plexus endothelium raises the possibility that the epithelial blood-cerebrospinal-fluid barrier plays an important role in the immunosurveillance of the central nervous system. PMID:8669469

  16. Three to Tango: MUC1 as a ligand for both E-selectin and ICAM-1 in the breast cancer metastatic cascade

    Directory of Open Access Journals (Sweden)

    Yue eGeng

    2012-07-01

    Full Text Available Cancer cell tethering and rolling on the vascular wall is facilitated by various selectin:glycoprotein interactions which lead to eventual extravasation and metastases. The aberrantly underglycosylated mucin MUC1 has been shown to both abundantly express selectin binding moieties (sialyl Lewis x and a and to consistently expose its core epitope. Flow cytometry was used to determine MUC1 expression on ZR-75-1 and MCF7 cells, while immunofluorescence microscopy was used to confirm the aberrant form of MUC1 and MUC1:ICAM-1 interactions. Each cell line was then perfused through combined E-selectin and ICAM-1 coated microtubes, as a model of the microvascular endothelium. ZR-75-1 and MCF7 were found to express abundant and low levels of underglycosylated MUC1, respectively. The rolling/adhesion profiles showed that ZR-75-1 cells, when compared to MCF7 cells, interact with E-selectin more efficiently resulting in sufficiently slow rolling velocities to form MUC1:ICAM-1 interactions thereby facilitating firm adhesion. The purpose and novelty of this work is the demonstration of the synergistic adhesion capabilities of MUC1 in the metastatic adhesion cascade, where the observed differential adhesion is consistent with the relative metastatic potential of the ZR-75-1 (highly metastatic and MCF7 (weakly metastatic cell lines.

  17. CKIP-1 ameliorates high glucose-induced expression of fibronectin and intercellular cell adhesion molecule-1 by activating the Nrf2/ARE pathway in glomerular mesangial cells.

    Science.gov (United States)

    Gong, Wenyan; Chen, Cheng; Xiong, Fengxiao; Yang, Zhiying; Wang, Yu; Huang, Junying; Liu, Peiqing; Huang, Heqing

    2016-09-15

    Glucose and lipid metabolism disorders as well as oxidative stress (OSS) play important roles in diabetic nephropathy (DN). Glucose and lipid metabolic dysfunctions are the basic pathological changes of chronic microvascular complications of diabetes mellitus, such as DN. OSS can lead to the accumulation of extracellular matrix and inflammatory factors which will accelerate the progress of DN. Casein kinase 2 interacting protein-1 (CKIP-1) mediates adipogenesis, cell proliferation and inflammation under many circumstances. However, whether CKIP-1 is involved in the development of DN remains unknown. Here, we show that CKIP-1 is a novel regulator of resisting the development of DN and the underlying molecular mechanism is related to activating the nuclear factor E2-related factor 2 (Nrf2)/antioxidant response element (ARE) antioxidative stress pathway. The following findings were obtained: (1) The treatment of glomerular mesangial cells (GMCs) with high glucose (HG) decreased CKIP-1 levels in a time-dependent manner; (2) CKIP-1 overexpression dramatically reduced fibronectin (FN) and intercellular adhesionmolecule-1 (ICAM-1) expression. Depletion of CKIP-1 further induced the production of FN and ICAM-1; (3) CKIP-1 promoted the nuclear accumulation, DNA binding, and transcriptional activity of Nrf2. Moreover, CKIP-1 upregulated the expression of Nrf2 downstream genes, heme oxygenase (HO-1) and superoxide dismutase 1 (SOD1); and ultimately decreased the levels of reactive oxygen species (ROS). The molecular mechanisms clarify that the advantageous effect of CKIP-1 on DN are well connected with the activation of the Nrf2/ARE antioxidative stress pathway. PMID:27481061

  18. Expression of platelet-endothelial cell adhesion molecule-1 in human umbilical vein endothelial cells by exposure to advanced glycosylation end products and inflammatory mediators

    Institute of Scientific and Technical Information of China (English)

    孟丹; 刘乃丰

    2003-01-01

    Objective To determine whether advanced glycosylation end products modified bovine serum albumin (AGEs-BSA) affects endothelial cell lateral junction protein, platelet-endothelial cell adhesion molecule-1 (PECAM-1) in the presence or absence of inflammatory mediators.Methods Cultured human umbilical vein endothelial cells (HUVECs) were exposed to AGEs-BSA for 6, 12, 24, and 36 hours, and exposed to AGEs-BSA glycosylated with different concentrations of glucose, tumor necrosis factord-α (TNF-α), interferon (IFN-γ), TNF-α+IFN-γ and AGEs-BSA+TNF-α for 24 hours, respectively. Expression of PECAM-1 mRNA was measured by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) with β-actin as an internal standard, and sequencing of RT-PCR products was performed to confirm the specificity of amplification for PECAM-1 gene. The endothelial cell surface expression of PECAM-1 was determined by flow cytometry (FCM).Results There were no significant changes in the expression of PECAM-1 mRNA and protein when the cells were exposed to AGEs-BSA with different concentrations or periods (P> 0.05). However, PECAM-1 expression was reduced in the cells treated with TNF-α, IFN-γ, TNF-α+IFN-γ and AGEs-BSA+TNF-α. The level of PECAM-1 treated with AGEs-BSA+TNF-α was lower than that of TNF-α treated alone (P<0.01).Conclusions AGEs-BSA had no effect on the expression of PECAM-1 mRNA and protein in cultured HUVEC. With the presence of inflammatory mediator TNF-α, AGEs-BSA decreased the level of PECAM-1, which might reduce the adhesion interaction between adjacent endothelial cells, enhance the permeability of endothelial cells, and might be implicated in the endothelial dysfunction and pathogenesis of atherosclerosis in patients with diabetes mellitus. The significance of this phenomenon in intracellular signal transduction remains to be determined.

  19. Effects of beraprost sodium on serum levels of soluble adhesion molecule-1 and C-reactive protein and urinary albumin excretion rate in patients with early diabetic nephropathy%贝前列素钠对早期糖尿病肾病患者血清可溶性细胞间黏附分子1、C反应蛋白及尿微量白蛋白排泄率影响的临床观察

    Institute of Scientific and Technical Information of China (English)

    黄娟; 张韶英; 段晓宇; 管斯斯

    2013-01-01

    Objective To observe the clinical efficacy of beraprost sodium on early stage of diabetic nephropathy(DN).Methods We measured serum levels of serum soluble intercelluhar adhesion molecule (sICAM)-1 in 27 cases with diabetes without nephropathy and 48 cases with early DN.Patients with early DN were randomly assigned into two treatment groups:the conventional treatment group and the beraprost sodium treatment group.Changes of sICAM-1 and C-reactive protein (CRP) levels and urinary albumin excretion rate (UAER) were measured in the two groups before and after treatment.Results The serum sICAM-1 levels in early DN patients was significantly higher than that of the diabetes without nephropathy group((1385 ± 171) g/ Lvs.(943 ± 167) g/L;t =1.034,P =0.002).There were no significant difference observed on levels of sICAM-1,CRP and UAER between the two treatment groups (P > 0.05).The level of sICAM-1 and CRP in the beraprost sodium treatment group was significantly lower than those before treatment (P < 0.05 or P < 0.01).The symptoms were significantly alleviated in both groups (P < 0.05 or P < 0.01),especially for the beraprost sodium treatment group(P < 0.05 or P < 0.01).Conclusion Patients with early DN have elevated serum sICAM-1 levels.Treatment of beraprost sodium has protective effect on early DN as it significantly decreases the serum levels of sICAM-1 and CRP in patients with early DN.%目的 观察贝前列素钠对早期糖尿病肾病(DN)患者的临床疗效.方法 测定27例糖尿病无肾病患者(糖尿病无肾病组)、48例早期DN(DN组)患者血清可溶性细胞间黏附分子1(sICAM-1)浓度,并将48例早期DN患者随机分为两组,常规治疗组和贝前列素钠治疗组,各24例,测定两组治疗前后sICAM-1、C反应蛋白(CRP)及尿微量白蛋白排泄率(UAER)的变化.结果 早期DN患者血清sICAM-1浓度[(1385±171) g/L与(943±167) g/L;t=1.034,P=0.002]明显高于糖尿病无肾病组.贝前列素钠治疗组与

  20. ICAM-1在儿童肿瘤中表达的临床意义%Expression and Clinical Significance of ICAM-1 in Pediatric Tumor

    Institute of Scientific and Technical Information of China (English)

    黄珂; 陈艳红

    2013-01-01

    目的 探讨细胞间黏附分子1(ICAM-1,CD54)在儿童肿瘤中的阳性表达率及其临床意义.方法 选择2008年1月1日-2012 年12 月31日收治的儿童肿瘤患者共85例和对照组20例.ICAM-1阳性表达,实体瘤35例采用免疫组织化学方法检测;白血病50例和对照组20例均采用流式细胞仪检测.比较白血病与对照组ICAM-1阳性表达率差异.结果 实体瘤中肝母细胞瘤ICAM-1检出100.0%(2/2),其他检出ICAM-1的实体肿瘤有淋巴瘤、横纹肌肉瘤、神经母细胞瘤、尤文氏肉瘤,而肾母细胞瘤和原始神经外胚层肿瘤未检出ICAM-1;急性淋巴细胞白血病和急性髓系白血病检出率分别为50.0%(10/20)和53.3%(16/30).急性白血病ALL 患儿骨髓细胞的 ICAM-1 阳性表达率为50.0%,与对照组比较无显著差异(P>0.05);AML ( M1、M2 和 M3) 组ICAM-1 阳性表达率为66.7%,显著高于对照组10.0 %(2/20)(P<0.05 );AML ( M4、M5) 组ICAM-1 阳性表达率为 33.3%,显著低于对照组75.0%(15/20) (P<0.05).结论 儿童肿瘤中ICAM-1表达存在差异,肝母细胞瘤、白血病患儿ICAM-1阳性率较高,临床上治疗时应考虑优先使用CIK 细胞免疫治疗.

  1. The influence of hyperbaric oxygenation to the adhesion molecules-1 of brain contusion patients%高压氧对脑挫裂伤患者粘附因子-1的影响

    Institute of Scientific and Technical Information of China (English)

    周政

    2012-01-01

    目的 研究高压氧对脑挫裂伤患者ICAM-1的影响.方法 分别于伤后4、24、48、72、96、120 h、6、7、8、9、10、11、13、23 d (高压氧治疗20 d后)酶联免疫法检测脑挫裂伤患者颈内静脉血ICAM-1含量.结果 脑挫裂伤患者的ICAM-1表达明显升高,高压氧治疗组ICAM-1表达和ICAM-1的峰值周期低于常规治疗对照组.结论 早期高压氧能通过降低脑挫裂伤患者的ICAM-1表达,缩短ICAM-1的峰值周期,减轻继发性脑损伤,达到脑保护和治疗作用.

  2. Differential effects of fenofibrate versus atorvastatin on the concentrations of E-selectin and vascular cellular adhesion molecule-1 in patients with type 2 diabetes mellitus and mixed hyperlipoproteinemia: a randomized cross-over trial

    Directory of Open Access Journals (Sweden)

    Otto Carsten

    2003-12-01

    Full Text Available Abstract Background Diabetic dyslipoproteinemia is characterized by hypertriglyceridemia, low HDL-cholesterol and often elevated LDL-cholesterol and is a strong risk factor for atherosclerosis. Adhesion molecule levels are elevated both in hyperlipoproteinemia and diabetes mellitus. It is unclear whether fibrate or statin therapy has more beneficial effects on adhesion molecule concentrations. Methods Atorvastatin (10 mg/d was compared to fenofibrate (200 mg/d each for 6 weeks separated by a 6 week washout period in 11 patients (6 male, 5 female; 61.8 ± 8.2 years; body mass index 29.8 ± 3.1 kg/m2 with type 2 diabetes mellitus (HbA1c 7.3 ± 1.1 % and mixed hyperlipoproteinemia using a randomized, cross-over design. Fasting blood glucose, HbA1c, lipid parameters, E-selectin, ICAM-1, VCAM-1, and fibrinogen concentrations were determined before and after each drug. Results Glucose and HbA1c concentrations remained unchanged during the whole study period. LDL cholesterol was reduced during atorvastatin therapy, triglycerides were lowered more effectively with fenofibrate. Comparison of pre- and postreatment concentrations of E-selectin showed a reduction during atorvastatin (-7 %, p = 0.11 and fenofibrate (-10 %, p Conclusions In addition to the different beneficial effects on lipid metabolism, both drugs appear to lower adhesion molecule plasma concentrations in a different manner in patients with type 2 diabetes and mixed hyperlipoproteinemia. Our observations should be confirmed in a larger cohort of such patients.

  3. Expression and significance of intercellular adhesion molecule-1 in retina of diabetic rats%细胞间黏附分子-1在糖尿病大鼠视网膜中的表达及意义

    Institute of Scientific and Technical Information of China (English)

    毛俊峰; 阎元奎; 艾育德; 刘双珍

    2004-01-01

    目的探讨细胞间黏附分子-1(ICAM-1)在糖尿病大鼠视网膜中的表达及ICAM-l多克隆抗体(ICAM-1Pab)的治疗作用. 方法Wistar大鼠40只随机分成4组:正常对照组(CON)、糖尿病组(DM)、糖尿病(ICAM-IPAb)组(DM ICAM-1PAb)和糖尿病(生理盐水)组(DM(salne)),每组10只.大鼠腹腔注射链脲佐菌素(STZ)诱发糖尿病模型.DM(ICAM-1PAb)组右眼结膜下注射ICAM-1PAb,连续1周.制作大鼠视网膜冰冻及石蜡切片分别行免疫组化SP染色和常规HE染色,对SP染色结果作计算机图像分析.结果ICAM-1在大鼠视网膜血管内皮细胞胞膜有表达.SP染色结果采用计算机图像分析系统处理.其中行DM组分别与CON组、DM(ICAM-IPAb)组比较有显著性差异(P<0.01).DM组视网膜血管内有较多附壁的白细胞.结论早期糖尿病大鼠视网膜ICAM-1表达上调,ICAM-1PAb通过阻断ICAM-1,抑制白细胞黏附,改善糖尿病大鼠视网膜微循环.

  4. Immunological Significance of the Detection of IL-17 and ICAM-1 in Systemic Lupus Erythematosus%系统性红斑狼疮血清IL-17和ICAM-1的检测及其免疫学意义

    Institute of Scientific and Technical Information of China (English)

    蒋巧雅; 迟秀文; 蓝宇萍

    2012-01-01

    Objective To explore the immunological machamism of interleukin-17(IL-17) and intercellular adhesion molecu-lar-l(ICAM-l) in the progress of Systemic Lupus Erythematosus(SLE). Methods According to valentijn method to determine the standard reference to collect 46 SLE patients in Longgang Central Hospital from May 2008 to August 2011, then classfied the activities of the 29 cases and 17 cases of remission. Venous blood was taken early in the morning and peripheral blood mononuclear cell culture supernatants was prepared. The sera of SLE patients and PMBC supernatant IL-17 and ICAM-1 was tesed by ELISA,at the same time the 42 healthy controls was taken. The parameters of IL-17 and ICAM-1 was compared with the commonly used laboratory parameters ANA.anti ds-DNA indicators. Results IL-17 and ICAM-1 levels in the serum of patients with SLE were 59. 12±5. 69 μmol/L and 494. 5±86. 51μg/L) significantly higher than SLE remission group of serum IL-17 and ICAM-1 levels 27. 13 ±3. 05 μmol/L and 185. 80 ± 32. 11 μg/L and normal control serum IL-17 and ICAM-1 levels 9. 50±1. 24 μmol/L and 91. 73±30. 10 μg/L, t value of 3. 859, P value 0. 021. Similarly,patients with SLEPBMC supernatant IL-17 and ICAM-1 levels 187. 76 ±27. 10 μmol/L and 582.20 ± 91.87 fig/L, significantly higher than SLE remission group PBMC supernatant IL-17 and ICAM-1 levels 45. 83 ±3. 97 pmol/L and 191. 73 ±30. 10 μg/L) and normal control group PBMC supernatant IL-17 and ICAM-1 levels 12. 64±2. 52 pmol/L and 214. 48±40. 07 μg/ L, t value 4. 051, P-value of 0. 028. And serum IL-17 and ICAM-1 levels 68. 36±6. 09 μmol/L and 600. 24 ± 91. 61 μg/L, t-value of 5. 909, P-value of 0. 024 in the ANA,antids-DNA-positive patients with SLE were Significantly higher than the serum IL-17 and ICAM-1 levels 24. 05±3. 17 μmol/L and 289. 55 ± 34. 81 μg/L, t value 2. 790, P value of 0. 038 in the ANA, anti ds-DNA negative SLE. And IL-17 and ICAM-1 were deceased significantly after effective therapy

  5. Plasmodium Falciparum: Adhesion Phenotype of Infected Erythrocytes Using Classical and Mini-Column Cytoadherence Techniques

    Directory of Open Access Journals (Sweden)

    N Kalantari

    2013-03-01

    Full Text Available Background: Cytoadherence of Plasmodium falciparum- infected erythrocytes to host cells is an impor­tant trait for parasite survival and has a major role in pathology of malaria disease. Infections with P. falciparum usually consist of several subpopulations of parasites with different adhesive proper­ties. This study aimed to compare relative sizes of various binding subpopulations of different P. falciparum isolates. It also investigated the adhesive phenotype of a laboratory P. falciparum line, A4, using different binding techniques.Methods: Seven different P. falciparum isolates (ITG, A4, 3D7 and four field isolates were cultivated to late trophozoite and schizont and then cytoadherence to cell differentiation 36 (CD36, intercellu­lar cell adhesion molecule-1 (ICAM-1, and vascular cell adhesion molecule (V-CAM and E-selectin were examined. The relative binding sizes of parasite subpopulations to human receptors were meas­ured by mini-column cytoadherence method. The adhesion phenotype of P. falciparum-A4 line was evaluated by in vitro static, flow-based and mini-column binding assays.Results: The relative binding size of ITG, A4 and 3D7 clones to a column made with CHO/ICAM-1 was 68%, 54% and 0%, respectively. The relative binding sizes of these lines to CHO/CD36 were 59.7%, 28.7% and 0%, respectively. Different field isolates had variable sizes of respective CD36 and ICAM1-binding subpopulations. A4 line had five different subpopulations each with different binding sizes.Conclusion: This study provided further evidence that P. falciparum isolates have different binding subpopulations sizes in an infection. Furthermore, measurement of ICAM-1 or CD36 binding subpopula­tions may practical to study the cytoadherence phenotypes of P. falciparum field isolates at the molecular level.

  6. Effects of Xuefu Zhuyu Capsule on the expression of serum ICAM-1 and ICAM-1 mRNA in renal tissues of AMI rats%血府逐瘀胶囊对AMI大鼠血清ICAM-1及肾脏组织ICAM-1 mRNA表达的影响

    Institute of Scientific and Technical Information of China (English)

    杜金行; 李腾飞; 宋威江; 廖江铨

    2014-01-01

    目的:观察血府逐瘀胶囊对大鼠心肌缺血后血清细胞间黏附分子-1(ICAM-1)含量及肾脏组织ICAM-1mRNA表达的影响.方法:将42只SD大鼠分为空白组8只、7d模型组8只、7d治疗组9只、14d模型组8只及14d治疗组9只,检测各组大鼠血清ICAM-1含量及肾脏组织ICAM-1 mRNA表达情况.结果:与空白组相比较,7及14d模型组大鼠血清ICAM-1含量及肾脏组织ICAM-1 mRNA表达均显著升高(P<0.01);经血府逐瘀胶囊治疗后,血清ICAM-1含量及肾脏组织ICAM-1 mRNA表达明显下降(P<0.05,P<0.01).结论:大鼠急性心肌梗死后血清炎症因子ICAM-1和肾组织中炎性因子ICAM-1 mRNA表达升高,血府逐瘀胶囊治疗可抑制循环及肾脏局部组织炎性因子表达.

  7. Expression profile of vascular cell adhesion molecule-1 (CD106) in inflammatory foci using rhenium-188 labelled monoclonal antibody in mice.

    Science.gov (United States)

    Kairemo, K J; Strömberg, S; Nikula, T K; Karonen, S L

    1998-06-01

    Rhenium (Re)-188 is a generator (W-188/Re-188) produced high energy beta-emitter suitable for radionuclide therapy (T1/2 is 16.9 hrs and Emax 2.1 MeV (range 11 mm)). We have labelled monoclonal antibody (MAb) raised against vascular cell adhesion molecule-1 (VCAM-1) with Re-188 using glucoheptonate chelation technique and SnCl2 as reducing agent. The labelling efficiency, free perrhenate and reduced Re were controlled with thin layer chromatography and the purification of Re-188-MoAbs was performed using gel filtration. Our results indicate that Re-188-labelled antibodies remain in vitro stable and the labelling purity is > 90%. We also have applied these Re-188-MoAbs for detection of inflammatory disease in a mouse. The effective half-lives of organs of interest after an injection of Re-188-anti-VCAM1 were as follows: blood 5.2 hr, kidney 4.7 hr, and liver 9.6 hr. Re-188-anti-VCAM-1 was found to accumulate mainly in kidney and liver. One hour after the injection, the kidney contained in average as high as 12.5% and the liver 2.8 ID/g tissue. After 6 hr, the kidney contained 5.5% ID/g and the liver 2.6% ID/g. At 24 hr, the kidney uptake was 0.5% ID/g and the liver uptake 0.8% ID/g, respectively. The inflamed foci, subcutaneous lesions in the footpad skin, were visualized using gamma camera. From the distribution data the uptakes in the inflamed foci as follows: at 1 hr 2.18 (inflammation) and 1.72% ID/g (control), at 6 hr 1.42 (inflammation) and 0.85% ID/g (control), and at 24 hr 0.17 (inflammation) and 0.084% ID/g (control), respectively. Anti-VCAM-1 MAb showed better targeting as compared to control MoAbs in inflammation (caused by E.coli lipoplysaccaride). In conclusion, Re-188 is suitable for MAb labelling, and MAb against VCAM-1 may be used for detection of local inflammatory disease. PMID:9762472

  8. 可溶性细胞间黏附分子-1在HBV感染不同免疫状态患者血清中变化%Relationship between the different immune status of HBV infection and the expression of sICAM-1

    Institute of Scientific and Technical Information of China (English)

    张艳平

    2012-01-01

    OBJECTIVE To study the expression and significances of the serum levels of soluble intercellular adhesion molecule-1 (sICAM-1) in patients with different immune status of hepatitis B virus (HBV) infection and Primary Hepatocel-lular Carcinoma (PHC). METHODS The patients of HBV infection were grouped into five teams, 60 cases were immune tolerance to HBV, 60 cases were immune clearance (30 cases with immunodeficiency in group A and another 30 cases with immunodeficiency in group B) with 30 patients in either groups, and 60 patients were diagnosed as PHC clinically. Serum samples were collected from these patients, and 30 healthy volunteers were taken as control for the study. The serum levels of sICAM-1 were measured by enzyme—linked immunosorbent assay (ELISA). RESULTS Serum levels of sICAM—1 in patients with immune clearance immunodeficiency (B) and PHC were significantly increased, and there was significant difference when compared with normal control (P 0.05). CONCLUSION Serum levels of sICAM-1 may reflect the disease progressed in patients with different immune status of HBV and have certainly valuable for clinical significance.%目的 观察乙型病毒性肝炎(HBV)感染不同免疫状态及HBV感染相关原发性肝癌(PHC)患者可溶性细胞间黏附分子-1 (sICAM-1)的变化及其意义.方法 利用ELISA法对60例HBV感染耐受、60例免疫清除、60例免疫不全(其中免疫不全A组30例,B组30例)及60例HBV感染性PHC患者进行血清sICAM-1检测,另选30例非HBV感染健康体检者作为正常对照组.结果 HBV感染不同免疫状态者中免疫清除、免疫不全A、免疫不全B及HBV感染相关PHC患者sICAM-1较正常对照组升高,差异有统计学意义(P<0.05);免疫耐受、免疫不全A组与正常对照组相比差异无统计学意义(P>0.05).结论 检测血清sICAM-1变化对判断HBV感染不同免疫状态病情变化具有一定的临床意义.

  9. Effects of ulinastatin on the mRNA expression of intercellular adhesion molecule-1 and P-selection in pulmonary tissue after ischemia reperfusion%乌司他丁对缺血再灌注肺组织细胞间黏附分子-1和P-选择素基因mRNA表达的影响

    Institute of Scientific and Technical Information of China (English)

    常忠路; 康炳玲; 陈庆伟

    2011-01-01

    OBJECTIVE To explore the effects of ulinastatin ( UTI ) on the mRNA expression of intercellular adhesion molecule ( ICAM ) - 1 and P - selection in pulmonary tissue after ischemia reperfusion. METHODS Eighteen New Zealand rabbits were randomly divided into 3 groups of 6 each: low potassium dextran ( LPD ) group, UTI group and control group. In vivo lung ischemia reperfusion model was established in rabbit, after hilum of left lung was clamped, the left lower lung lobe was stored at 10℃ in a special made lung preservation container for 2 hours and reperfused for another 2 hours. In LPD group and UTI group the left lower lobe was perfused with LPD solution or LPD solution contained ulinastatin respectively, without anything perfused in control group. The pulmonary tissue was obtained at three time intervals and the mRNA expression of ICAM - 1 and P - selection in pulmonary tissue was measured using RT - PCR technique. RESULTS The mRNA expression of ICAM - 1 at 2 hours after ischemia and 2 hours after perfusion in UTI group was significantly lower than that in LPD group and control group. The P - selection mRNA expression at 2 hours after perfusion in LPD group and control group was significantly higher than pre - ischemia and 2 hours after clamping hilum of left lung.There was no such significant difference in UTI group. CONCLUSION UTI can inhibit the upregulation of the mRNA expression of ICAM -1 and P -selection after ischemia reperfusion in pulmonary tissue, so it is profitable for pulmonary protection.%目的 探讨乌司他丁(UTI)对在体缺血再灌注后肺组织细胞间黏附分子(ICAM)-1和P-选择素基因mRNA表达的影响.方法 新西兰兔18只随机分为3组:低钾右旋糖酐液(LPD)组、UTI组和对照组.建立兔在体肺缺血冷存再灌注模型,阻断左肺门后将左肺下叶在体冷存于10℃肺保存器内2 h,再灌注2 h.LPD组灌注LPD液,UTI组灌注含UTI的LPD液,对照组不灌注肺保护液.分别

  10. Effects of Interleukin-1β,-1Rα on the Expression of Matrix Metalloproteinases-9 and Intercellular Adhesion Molecule-1 in the Embryo and Endometrium Co-Culture System%白细胞介素-1β,-1Rα对胚胎-内膜共培养体系分泌基质金属蛋白酶-9/细胞间黏附分子-1的影响

    Institute of Scientific and Technical Information of China (English)

    张宁; 刘萍; 郝翠芳; 王昕荣

    2012-01-01

    epithelial cells were collected and the endometrial cells were primarily cultured.There were 7 copies primary endometrial cells were successful cultured and were inoculated into 35 holes respectively.Control group were 5 hole cells without any treatment (n=5 × 7).30 holes was divided into 6 groups according to different concentrations of IL-1β and different raio of IL-1β3+IL-1Ra.3 groups were GⅡ with 1 ng/mL IL-1β,10 ng/mL IL1β and 100 ng/mL IL-1β,3 groups were G Ⅱ with 1 ng/mL IL-1β+ 10 μg/mL IL 1Rα,10 ng/mL IL-1β+ 10μg/mL IL-1Rα and 100 ng/mL IL 1β+ 10 μg/mL IL-1Rα (n=5 × 7).8 cell embryos were co-cultured with endometrial glandular epithelial cells in different media (6 embryos each hole).Supernatant were collected after 48 h co-culture,and the levels of matrix metalloproteinase-9 (MMP-9) / intercellular adhesion molecule-1 (ICAM-1) were measured by ELISA.Results Expressions of MMP-9 / ICAM 1 were significantly increased in 1 ng/mL IL-1β group and 10 ng/mL IL-1β group compared with those in control group respectively (P<0.05).While expression of MMP 9/ICAM1 levels had no significant differences in 1 ng/mL IL-1β group and in 10 ng/mL IL-1β group,and also in 100 ng/mL IL-1β group and in control group (P>0.05).MMP-9/ICAM-1 levels were significant decreased in 10 ng/mL IL-1β+ 10 μg/mL IL-1Ra group compared with those control group (P<0.05); While expression of MMP-9/ICAM-1 levels had no significant differences in 1 ng/mL IL-1β+ 10 μg/mL IL-1Ra group and in control group,and also had no significant in 100 ng/mL IL-1β+10 μg/mL IL-1Ra group and in control group (P>0.05).They also had no significant difference in 1 ng/mL IL-1β+10 μg/mL IL-1Ra group compared with those in 100 ng/mL IL-1β +10 μg/mL IL-1Ra group (P>0.05).Conclusions Appropriate proportion of IL-1β and IL-1Rα can regulate embryo implantation.

  11. Levels of soluble adhesion molecules in patients with various clinical presentations of coronary atherosclerosis

    Institute of Scientific and Technical Information of China (English)

    LU Hui-he; SHENG Zheng-qiang; WANG Yi; ZHANG Li

    2010-01-01

    Background Adhesion molecules play an important role in the development and progression of coronary atherosclerosis. The aim of this study was to compare concentrations of soluble forms of adhesion molecules in patients with different clinical presentations of coronary artery disease (CAD).Methods One hundred and twenty-eight patients with CAD were divided into three groups; the first group was acute myocardial infarction group (AMI group, n=45), the second group was unstable angina pectoris group (UAP group, n=48),the third group was stable angina pectoris group (SAP group, n=35). We compared them with patients with normal coronary arteries (control group, n=31). The serum levels of vascular cell adhesion molecule (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), E-selectin and P-selectin were measured in all subjects.Results The serum level of VCAM-1 in the AMI group was significantly higher than in the UAP, SAP and control groups (P <0.01). The level in the UAP group was significantly higher than the SAP group and control group (P <0.01) and the level in the SAP group was significantly higher than in the control group (P <0.01). The serum ICAM-1 level was significantly elevated in the AMI, UAP and SAP groups as compared to the control group (P <0.01). The levels of serum E-selectin and P-selectin in the AMI and UAP groups were significantly higher than in the SAP and control groups (P<0.01).Conclusions Increased levels of VCAM-1 and ICAM-1, E-selectin and P-selectin, as markers of inflammation, showed the importance of inflammatory processes in the development of atherosclerosis and clinical expression of CAD. Soluble ICAM-1, VCAM-1, E-selectin and P-selectin concentrations are useful indicators of the presence of atherosclerosis and the severity of CAD clinical presentation.

  12. The protective effects and cerebral cortex expression of MMP-9 and ICAM-1 of simvastatin on hypoxic-ischemic brain damage in neonatal rats%探讨辛伐他汀对新生大鼠缺氧缺血性脑病的保护作用及其对大脑皮质MMP-9和ICAM-1表达的影响

    Institute of Scientific and Technical Information of China (English)

    罗勇; 韦红; 王燕; 彭梅

    2014-01-01

    a day for 7 d in group I and II , in simvastatin group ,simvastatin was administered ip instead of NS . Brain damage was evaluated by survival rate and the capacity of learning and memory using Y-Maze test . Matrix metalloproteinases9 (MMP-9) and intercellular adhesion molecule-1 (ICAM-1) in the bilateral cortex was detected at24 h, 48 h and 72 h in HIBD rats treated with simvastatin by Western blotting. Results (1)The survival rate on the 28th day after hypoxia or sham operation was significant lower in control group than that in the other groups(P<0 05).(2)The capacity text of learning and memory in the control group was under the target rate and signifi-cantly lower than that in the other groups(P<0.05).(3) Simvastatin inhibited the expression of MMP-9 and ICAM-1 in a time de-pendent manner and the effect of 1 mg/ml and 10 mg/ml has significant differences (P<0.05). Conclusion Simvastatin can protect brain from hypoxic-ischemic injury in rats by inhibiting the protein expression of MMP-9 and ICAM-1.

  13. Effects of trans-3,5,4′-trimethoxystilbene on the expressions of NO,ICAM-1 and NF-κB in human umbilical vein endothelial cells induced by lipopolysaccharide in vitro%白藜芦醇衍生物 TMS 对脂多糖诱导血管内皮细胞表达 NO、ICAM-1和 NF-κB 的影响

    Institute of Scientific and Technical Information of China (English)

    付海燕; 胡占升; 杜红阳

    2015-01-01

    Objective To explore the effects of trans-3,5,4′-trimethoxystilbene (TMS)on the expressions of NO, intercellular adhesion molecule-1 (ICAM-1)and nuclear factor-κB (NF-κB)in human umbilical vein endothelial cells (HUVEs)induced by lipopolysaccharide (LPS)in vitro.Methods The cell viabilities influenced by the different concentrations of TMS were assessed by CCK-8 assay.The cells were divided into the control group (CON group), LPS group,low-concentration TMS plus LPS group,medium-concentration TMS plus LPS group,high-concentration TMS plus LPS group and ammonium pyrrolidine dithiocarbamate (PDTC)plus LPS group.HUVEs were pretreated with the different concentrations of TMS and 10 μmol/L PDTC,and then were stimulated with 0.1 μg /mL LPS.After incubation,the level of NO was determined by Griess assay.The mRNA expressions of ICAM-1 and NF-κB p65 were detected by Real-time PCR,the protein expressions of ICAM-1,NF-κB p65 and IκBαby Western blotting assay,and the protein expressions of ICAM-1 and NF-κB p65 by immunocytochemetry assay.Results There was little effect of low-concentration TMS (5 or 10 μmol/L)on the cell viability,but the cell viability decreased significantly when trea-ted with high-concentration TMS (50 or 100 μmol/L)in time-or concentration-dependent manners.Griess results showed that the level of NO in the low-,medium-and high-concentration TMS plus LPS groups and PDTC plus LPS group decreased compared with that in LPS group (P <0.05 ).The results of Real-time PCR and Western blotting showed that compared with LPS group and CON group,there were significant difference of mRNA and protein expressions of ICAM-1 and NF-κB p65 in medium-concentration TMS plus LPS group and PDTC plus LPS group (P <0.05;P <0.01).Furthermore,there were nuclear expressions of NF-κB p65 protein in medium-concentration TMS plus LPS group,PDTC plus LPS group and LPS group except for CON group.The protein expression of IκBαdecreased significantly in LPS group compared

  14. Effect of a diet and exercise intervention on oxidative stress, inflammation and monocyte adhesion in diabetic men.

    Science.gov (United States)

    Roberts, Christian K; Won, Dean; Pruthi, Sandeep; Lin, San San; Barnard, R James

    2006-09-01

    Diabetes increases the risk of coronary artery disease. We examined the effects of lifestyle modification on key contributing factors to atherogenesis, including oxidative stress, inflammation and cell adhesion. Diabetic men (N=13) were placed on a high-fiber, low-fat diet in a 3-week residential program where food was provided ad libitum and daily aerobic exercise was performed. In each subject, pre- and post-intervention fasting blood was drawn for circulating levels of serum lipids, glucose and insulin, oxidative stress marker 8-isoprostaglandin F2alpha (8-iso-PGF2alpha), the inflammatory protein C-reactive protein (CRP), and soluble intracellular adhesion molecule (sICAM)-1 and sE-selectin as indicators of endothelial activation. Using subject sera and human aortic endothelial cell (HAEC) culture systems, serum-induced monocyte adhesion, ICAM-1, vascular cell adhesion molecule-1 (VCAM-1) and cell surface abundance, and monocyte chemotactic protein-1 (MCP-1) production were determined. Nitric oxide (NO), superoxide, and hydrogen peroxide production were measured in vitro by fluorometric detection. After 3 weeks, significant reductions (pfasting serum glucose (157.5+/-10.1 mg/dL versus 126.7+/-8.7 mg/dL), insulin (33.8+/-4.0 microU/ml versus 23.8+/-3.4 microU/ml), homeostasis model assessment for insulin resistance, 8-iso-PGF2alpha, CRP, sICAM-1, and sE-selectin were noted. In vitro, serum-stimulated monocyte adhesion, cellular ICAM-1 and VCAM-1 expression (p<0.05), and fluorometric detection of superoxide and hydrogen peroxide production decreased, while a concomitant increase in NO production was noted (all p<0.01). A combination of diet and exercise ameliorates oxidative stress, inflammation, and monocyte-endothelial interaction. Intensive lifestyle modification may improve novel CAD risk factors in men with diabetes. PMID:16616795

  15. Differential modulation of IL-1-induced endothelial adhesion molecules and transendothelial migration of granulocytes by G-CSF.

    Science.gov (United States)

    Eissner, G; Lindner, H; Reisbach, G; Klauke, I; Holler, E

    1997-06-01

    Granulocyte colony stimulating factor (G-CSF) is widely used for mobilization of haemopoietic stem cells into the peripheral blood. However, little is known about the mechanisms involved in mobilization and the immune modulatory effects of this growth factor. In this report we show that G-CSF down-regulated intercellular adhesion molecule 1 (ICAM-1) induced by Interleukin-1 (IL-1) on human endothelial cells. Interestingly, the G-CSF-mediated down-modulation of IL-1-induced ICAM-1 appeared to be biphasic. In pharmacological concentrations (> 300 ng/ml), and in dose ranges of plasma G-CSF levels above that of nonfebrile healthy individuals (30 pg/ml), a significant decrease in surface ICAM-1 could be observed. This could be explained, at least in part, by an increased autocrine G-CSF production by endothelial cells in response to IL-1 and exogenous G-CSF. In contrast to ICAM-1, IL-1-triggered VCAM-1 expression was superinduced by G-CSF with the optimal concentration of 30 pg/ml. To evaluate the functional significance of these findings, 51Cr adhesion assays with peripheral blood mononuclear cells (PBMC) or granulocytes known to lack the VCAM-1 counter-receptor very late antigen 4 (VLA-4) and IL-1-stimulated endothelial cells, in the presence or absence of G-CSF, were performed. G-CSF could not inhibit the IL-1-induced adhesion of PBMC to endothelial cells, which may be due to the differential adhesion molecule modulation. In contrast, granulocyte adhesion induced by IL-1 could effectively be blocked by co-incubation with G-CSF. Finally, G-CSF also inhibited transendothelial migration of granulocytes through IL-1-activated endothelial cells in a concentration-dependent manner.

  16. Highly sensitivity adhesion molecules detection in hereditary haemochromatosis patients reveals altered expression.

    LENUS (Irish Health Repository)

    Norris, S

    2012-02-01

    Several abnormalities in the immune status of patients with hereditary haemochromatosis (HH) have been reported, suggesting an imbalance in their immune function. This may include persistent production of, or exposure to, altered immune signalling contributing to the pathogenesis of this disorder. Adhesion molecules L-, E- and P-Selectin, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) are some of the major regulators of the immune processes and altered levels of these proteins have been found in pathological states including cardiovascular diseases, arthritis and liver cancer. The aim of this study was to assess L-, E- and P-Selectin, ICAM-1 and VCAM-1 expression in patients with HH and correlate these results with HFE mutation status and iron indexes. A total of 139 subjects were diagnosed with HH (C282Y homozygotes = 87, C282Y\\/H63D = 26 heterozygotes, H63D homozygotes = 26), 27 healthy control subjects with no HFE mutation (N\\/N), 18 normal subjects heterozygous for the H63D mutation served as age-sex-matched controls. We observed a significant decrease in L-selectin (P = 0.0002) and increased E-selectin and ICAM-1 (P = 0.0006 and P = 0.0059) expression in HH patients compared with healthy controls. This study observes for the first time that an altered adhesion molecules profile occurs in patients with HH that is associated with specific HFE genetic component for iron overload, suggesting that differential expression of adhesion molecules may play a role in the pathogenesis of HH.

  17. Cell adhesion molecules involved in the leukocyte recruitment induced by venom of the snake Bothrops jararaca

    Directory of Open Access Journals (Sweden)

    Stella R. Zamuner

    2002-01-01

    Full Text Available It has been shown that Bothrops jararaca venom (BjV induces a significant leukocyte accumulation, mainly neutrophils, at the local of tissue damage. Therefore, the role of the adhesion molecules intercellular adhesion molecule-1 (ICAM-1, LECAM-1, CD18, leukocyte function-associated antigen-1 (LFA-1 and platelet endothelial cell adhesion molecule-1 (PECAM-1 on the BjV-induced neutrophil accumulation and the correlation with release of LTB4, TXA2, tumor necrosis factor-α, interleukin (IL-1 and IL-6 have been investigated. Anti-mouse LECAM-1, LFA-1, ICAM-1 and PECAM-1 monoclonal antibody injection resulted in a reduction of 42%, 80%, 66% and 67%, respectively, of neutrophil accumulation induced by BjV (250 μg/kg, intraperitoneal injection in male mice compared with isotype-matched control injected animals. The anti-mouse CD18 monoclonal antibody had no significant effect on venom-induced neutrophil accumulation. Concentrations of LTB4, TXA2, IL-6 and TNF-α were significant increased in the peritoneal exudates of animals injected with venom, whereas no increment in IL-1 was detected. This results suggest that ICAM-1, LECAM-1, LFA-1 and PECAM-1, but not CD18, adhesion molecules are involved in the recruitment of neutrophils into the inflammatory site induced by BjV. This is the first in vivo evidence that snake venom is able to up-regulate the expression of adhesion molecules by both leukocytes and endothelial cells. This venom effect may be indirect, probably through the release of the inflammatory mediators evidenced in the present study.

  18. 哮喘病人外周血单个核细胞ICAM-1 mRNA表达测定%Expression of ICAM-1 mRNA on peripheral blood mononuclear cells in asthma

    Institute of Scientific and Technical Information of China (English)

    金淑贤; 张祖贻; 高平

    2002-01-01

    目的:探讨细胞间粘附分子-1(ICAM-1)在哮喘炎症反应中的作用,进一步了解哮喘发病机制.方法:采用免疫组织化学和RT-PCR方法检测10例支气管哮喘发作患者和10例正常人外周血单个核细胞(PBMCs)ICAM-1表达.结果:哮喘患者PBMCs ICAM-1ICAM-1 mRNA均较正常对照组增高(P<0.05),哮喘患者PBMCs ICAM-1ICAM-1 mRNA表达成正相关.结论:ICAM-1参与哮喘炎症反应的发生.

  19. 血清晚期氧化蛋白产物、细胞间黏附分子1、白介素1β与糖尿病肾病的关系及辛伐他汀的干预研究%Association of Serum Advance Oxidative Protein Products,Intercellular Adhesion Molecule 1,and Interleukin-1β with Diabetic Kidney Disease and the Intervention with Simvastatin

    Institute of Scientific and Technical Information of China (English)

    李弋南; 金建生; 张燕林

    2012-01-01

    Objective To study the clinical significance of serum advance oxidative protein products ( AOPP ), intercellular adhesion moleculel ( ICAM - 1 ), and interleukin -1(3(IL-I(3)in patients with diabetic kidney disease ( DN ) and explore the therapeutic mechanism of simvastatin. Methods Eighty - nine patients with type 2 diabetic mellitus ( T2DM ) were divided into three groups: normal albumin urine group ( n = 31 ), microamount albumin urine group ( n = 28 ), and dominancy albumin urine group ( n = 30 ) based on the urinary albumin excretion rate ( UAER ), and 30 healthy subjects were used as controls. AOPP, ICAM - 1, and IL - 1 (3 were measured by enzyme - linked - immuno sorbent assay ( ELISA ) in the T2DM patients and the control group. Patients with microamount albumin urine and dominancy albumin urine were treated with simvasts-tin. Results The serum AOPP, ICAM - 1, and IL - 1 (3 levels in the three T2DM groups were significantly higher than in control group ( all P < 0. 05 ), and higher in the dominancy albumin urine group than those in the microamount albumin urine and normal albumin urine groups ( both P < 0. 01 ). The serum AOPP, ICAM - 1, and IL - 1 (3 levels in the microamount albumin u-rine group were significantly higher than in the normal albumin urine group ( P < 0. 05 ), and the serum AOPP, ICAM - 1, and IL - 1(3 levels were positively correlated ( P <0. 01 ). The serum AOPP, ICAM - 1, and IL - 1(3 levels were positively correlated with UAER, respectively ( P <0. 01 ). After treatment with simvastatin, the serum UAER, AOPP, ICAM - 1, and IL -1 (3 levels significantly decreased in the microamount albumin urine group and dominancy albumin urine group ( all P < 0. 05 ). Conclusion The plasma levels of AOPP, ICAM - 1 and IL - 1 (3are sensitive markers for the early diagnosis of DN, and are associated positively with the onset and progression of DM. Through antioxidation and the inhibition of subclinical inflammation,simvastatin may directly or indirectly

  20. Impaired sensitivity to beta 2 integrin-blocking in ICAM-1-mediated neutrophil migration in ulcerative colitis

    DEFF Research Database (Denmark)

    Vainer, B; Brimnes, J; Claesson, M H;

    2001-01-01

    BACKGROUND: Factors influencing the directed migration of neutrophils into colonic tissue in ulcerative colitis (UC) are poorly described. ICAM-1 has recently been shown to possess chemotactic properties, and the aim of this study was to evaluate the involvement of beta 2 integrins in this ICAM-1......-mediated migration. METHODS: The chemotactic effect of ICAM-1 on neutrophils isolated from 13 UC patients and 17 healthy volunteers was studied in microchemotaxis chambers. Physiological concentrations of ICAM-1 (0.05-500 pM) were separated from neutrophils by nitrocellulose filters, and cell migration...... was evaluated using the leading front technique. beta 2 integrins on neutrophils were blocked with antibodies to CD11a, CD11b, CD11c and CD18, and migration towards ICAM-1 was examined. RESULTS: Migration towards ICAM-1 was equal for UC and control neutrophils, showing a bell-shaped ICAM-1 dosemigratory...

  1. 肝癌组织中ICAM-1的表达和意义%Expression and Significance of ICAM-1 in Hepatocellular Carcinoma

    Institute of Scientific and Technical Information of China (English)

    刘菊; 熊枝繁

    2005-01-01

    目的研究细胞间黏附分子-1(1CAM-1)在原发性肝癌中的临床意义.方法以免疫组化方法结合全自动图像分析观察40例肝细胞癌组织及其癌旁组织和28例肝硬化组织中ICAM-1的表达.结果40例肝细胞癌组织ICAM-1表达阳性率为80.0%(32/40)、癌旁组织为57.5%(23/40)、肝硬化为53.6%(15/28),阳性率与组织学分类相关.肝癌组织中ICAM-1含量明显高于癌旁及肝硬化组织(P<0.05),转移组肝癌中ICAM-1的含量明显高于非转移组(P<0.05),而癌旁及肝硬化组织中表达差异无显著性(P>0.05).结论肝癌组织中高度表达ICAM-1,ICAM-1有可能作为判断肝硬化及肝癌发展程度及预后的指标之一.

  2. Low-Level Laser Therapy Attenuates LPS-Induced Rats Mastitis by Inhibiting Polymorphonuclear Neutrophil Adhesion

    OpenAIRE

    Wang, Yueqiang; HE, Xianjing; HAO, Dandan; Yu, Debin; LIANG, Jianbin; QU, Yanpeng; Sun, Dongbo; Yang, Bin; YANG, Keli; Wu, Rui; WANG, Jianfa

    2014-01-01

    ABSTRACT The aim of this study was to investigate the effects of low-level laser therapy (LLLT) on a rat model of lipopolysaccharide (LPS)-induced mastitis and its underlying molecular mechanisms. The rat model of mastitis was induced by inoculation of LPS through the canals of the mammary gland. The results showed that LPS-induced secretion of IL-1β and IL-8 significantly decreased after LLLT (650 nm, 2.5 mW, 30 mW/cm2). LLLT also inhibited intercellular adhesion molecule-1 (ICAM-1) expressi...

  3. ICAM-1蛋白和mRNA在慢性乙型肝炎肝组织中的表达%Expression of ICAM-1 protein and mRNA in the liver of patients with chronic hepatitis B

    Institute of Scientific and Technical Information of China (English)

    张绪清; 顾长海

    2000-01-01

    目的:探讨肝组织细胞间粘附分子-1(ICAM-1)表达在慢性乙型肝炎(CHB)发病机制中的作用.方法:用原位杂交和免疫组织化学技术检测11例正常人和50例慢性HBV感染者肝内ICAM-1 mRNA和蛋白表达情况.结果:正常人和慢性无症状HBsAg携带者肝细胞无ICAM-1 mRNA和ICAM-1表达,CHB患者肝细胞ICAM-1 mRNA和ICAM-1表达增强,阳性肝细胞多分布在汇管区周围和腺泡内炎症坏死区域;重度CHB患者肝细胞ICAM-1 mRNA和ICAM-1表达显著强于中、轻度CHB患者(P< 0.05);肝细胞ICAM-1表达强度与肝组织炎症活动度呈显著正相关(P< 0.01);肝细胞ICAM-1表达强的患者肝功能显著差于ICAM-1表达弱者(P< 0.05).结论:肝细胞ICAM-1表达在慢性乙型肝炎肝细胞坏死中起重要作用,肝细胞ICAM-1表达水平能较好反映其肝损害程度和肝功能状况.

  4. SODs are involved in the regulation of ICAM-1 expression in human melanoma and endothelial cells.

    Science.gov (United States)

    Morandini, R; Boeynaems, J M; Duhant, X; Jacquemotte, F; Kinnaert, E; Ghanem, G

    1999-11-01

    It is well known that ICAM-1 expression can be stimulated by TNF and by oxidative stress, via the activation of specific transcription factors. Two of these--NFkappaB and AP-1--can also be activated by reactive oxygen species, including the superoxide anion (also produced under TNF challenge). The latter is inactivated by superoxide dismutase of which two forms exist: Cu/Zn-SOD (cytoplasmic) and Mn-SOD (mitochondrial). We investigated whether superoxide anion direct generation or accumulation through specific SOD inhibition, may affect ICAM-1 expression in human melanoma and endothelial cells. Our results show a 20-50% increase in both SOD activities when cells were exposed to TNF or to an oxidative stress produced by Paraquat (a generator of superoxide anion radicals), both in terms of enzymes activity (zymogram) and protein levels (Western blotting and ELISA). Either with TNF or Paraquat, we could measure a significant increase of ICAM-1 expression with maxima ranging from 140 to 200%, depending on the cell line. Specific inhibition of Cu/Zn-SOD activity by DTIC (diethyldithiocarbamic acid), in presence of Paraquat or TNF, was followed by an upregulation of ICAM-1 expression (60 and 20%, respectively). In contrast, the addition of a SOD mimetic (MnTMPyP) completely inhibited Paraquat-stimulated ICAM-1 expression in melanoma cells and significantly decreased it in HUVEC (50%). In presence of TNF however, the same SOD mimetic inhibited TNF-stimulated ICAM-1 expression by 25% in melanoma and 17% in endothelial cells. In conclusion, these data provide evidence that melanoma and endothelial cells exposure to TNF or oxidative stress results in a significant increase of both Mn- and Cu/Zn-SOD activities. This increase seems to be associated with a reduction in the stimulation of ICAM-1 expression by TNF or oxidative stress. PMID:10644010

  5. Effect of Linomide on adhesion molecules, TNF-alpha, nitrogen oxide, and cell adhesion.

    Science.gov (United States)

    Abdul-Hai, A; Hershkoviz, R; Weiss, L; Lider, O; Slavin, S

    2005-02-01

    Linomide (quinoline-3-carboxamide) is an immunomodulator with anti-inflammatory effects in rodents with autoimmune diseases. Its mode of action still remains to be elucidated. We hypothesized that an investigation of T cell interactions with the extracellular matrix (ECM), composed of glycoproteins such as fibronectin (FN) and laminin (LN), might provide better understanding of their in vivo mode of action in extravascular inflammatory sites. We examined the effect of Linomide on T cell adhesion to intact ECM, and separately to LN, and FN, and on the release and production of tumor necrosis factor (TNFalpha) and nitrogen oxide (NO) in relation to adhesive molecules in non-obese diabetic (NOD) female spleen cells, focusing on intracellular adhesion molecule-1 (ICAM-1) and CD44. NOD female mice that developed spontaneous autoimmune insulitis, which destroys pancreatic islets and subsequently leads to insulin-deficient diabetes mellitus, were studied. Linomide, given in the drinking water or added to tissue cultures in vitro, inhibited the beta1 integrin-mediated adhesion of T cells to ECM, FN and LN, as well as the production and release of TNFalpha and NO, which play a major role in the induction and propagation of T cell-mediated insulitis. In addition, exposure of T cells to Linomide resulted in increased expression of CD44 and ICAM-1 molecules on spleen cells of Linomide-treated mice; such an increase in adhesion molecule expression may lead to more effective arrest of T cell migration in vivo. The regulation of T-cell adhesion, adhesion receptor expression, and inhibition of TNFalpha and NO secretion by Linomide may explain its beneficial role and provide a new tool for suppressing self-reactive T cell-dependent autoimmune diseases. PMID:15652754

  6. Effect of irradiation on gene expression of rat liver adhesion molecules. In vivo and in vitro studies

    Energy Technology Data Exchange (ETDEWEB)

    Moriconi, Federico; Malik, Ihtzaz; Ahmad, Ghayyor; Dudas, Joszef; Ramadori, Giuliano [Dept. of Gastroenterology and Endocrinology, Goettingen Univ. (Germany); Rave-Fraenk, Margret; Vorwerk, Hilke; Hille, Andrea; Hess, Clemens Friedrich; Christiansen, Hans [Dept. of Radiotherapy, Goettingen Univ. (Germany)

    2009-07-15

    Background and purpose: Migration of leukocytes into tissue is a key element of innate and adaptive immunity. An animal study showed that liver irradiation, in spite of induction of chemokine gene expression, does not lead to recruitment of leukocytes into the parenchyma. The aim of this study was to analyze gene expression of adhesion molecules, which mediate leukocyte recruitment into organs, in irradiated rat liver in vivo and rat hepatocytes in vitro. Material and methods: Rat livers in vivo were irradiated selectively at 25 Gy. Isolated hepatocytes in vitro were irradiated at 8 Gy. RNA extracted within 48 h after irradiation in vivo and in vitro was analyzed by real-time PCR (polymerase chain reaction) and Northern blot. Adhesion molecule concentration in serum was measured by ELISA (enzyme-linked immunosorbent assay). Cryostat sections of livers were used for immunohistology. Results: Significant radiation-induced increase of ICAM-1 (intercellular adhesion molecule-1), VCAM-1 (vascular cell adhesion molecule-1), JAM-1 (junctional adhesion molecule-1), {beta}{sub 1}-integrin, {beta}{sub 2}-integrin, E-cadherin, and P-selectin gene expression could be detected in vivo, while PECAM-1 (platelet-endothelial cell adhesion molecule-1) gene expression remained unchanged. In vitro, {beta}{sub 1}-integrin, JAM-1, and ICAM-2 showed a radiation-induced increased expression, whereas the levels of P-selectin, ICAM-1, PECAM-1, VCAM-1, Madcam-1 (mucosal addressin cell adhesion molecule-1), {beta}{sub 2}-integrin, and E-cadherin were downregulated. However, incubation of irradiated hepatocytes with either tumor necrosis factor-(TNF-){alpha}, interleukin-(IL-)1{beta}, or IL-6 plus TNF-{alpha} led to an upregulation of P-selectin, ICAM-1 and VCAM-1. Conclusion: The findings suggest that liver irradiation modulates gene expression of the main adhesion molecules in vivo and in cytokine-activated hepatocytes, with the exception of PECAM-1. This may be one reason for the lack of

  7. The carbon monoxide releasing molecule (CORM-3) inhibits expression of vascular cell adhesion molecule-1 and E-selectin independently of haem oxygenase-1 expression

    NARCIS (Netherlands)

    Song, H.; Bergstrasser, C.; Rafat, N.; Hoeger, S.; Schmidt, M.; Endres, N.; Goebeler, M.; Hillebrands, J. L.; Brigelius-Flohe, R.; Banning, A.; Beck, G.; Loesel, R.; Yard, B. A.

    2009-01-01

    Background and purpose: Although carbon monoxide (CO) can modulate inflammatory processes, the influence of CO on adhesion molecules is less clear. This might be due to the limited amount of CO generated by haem degradation. We therefore tested the ability of a CO releasing molecule (CORM-3), used i

  8. Degraded carrageenan causing colitis in rats induces TNF secretion and ICAM-1 upregulation in monocytes through NF-kappaB activation.

    Directory of Open Access Journals (Sweden)

    Claudine Benard

    Full Text Available Carrageenan (CGN is a high molecular weight sulphated polysaccharide derived from red seaweeds. In rodents, its degraded forms (dCGN can induce intestinal inflammation associated with macrophage recruitment and activation. The aim of this study was: 1 to analyze the size-dependent effects of dCGN on colon inflammation in vivo, and 2 to correlate these effects with monocyte/macrophage proliferation, cytokine production and expression of various cell surface antigens including ICAM-1 adhesion molecule. Peripheral blood monocytes (PBM and THP-1 monocytic cells were cultured in the presence of either 10 or 40 kDa, dCGN. The 40 kDa, but not the 10 kDa dCGN, induced colitis in in vivo. Degraded CGN inhibited THP-1 cell proliferation in vitro, arresting the cells in G1 phase. In addition, dCGN increased ICAM-1 expression in both PBM and THP-1 cells with a major effect seen after 40 kDa dCGN exposure. Also, dCGN stimulated monocyte aggregation in vitro that was prevented by incubation with anti-ICAM-1 antibody. Finally, dCGN stimulated TNF-alpha expression and secretion by both PBM and THP-1 cells. All these effects were linked to NF-kappaB activation. These data strongly suggest that the degraded forms of CGN have a pronounced effect on monocytes, characteristic of an inflammatory phenotype.

  9. Association of TLR2 S450S and ICAM1 K469E polymorphisms with polycystic ovary syndrome (PCOS) and obesity.

    Science.gov (United States)

    Ojeda-Ojeda, Miriam; Martínez-García, M Ángeles; Alpañés, Macarena; Luque-Ramírez, Manuel; Escobar-Morreale, Héctor F

    2016-02-01

    Toll-like receptors (TLRs) are activated by inflammatory stimuli and influence endothelial functions, contributing to the pathogenesis of atherosclerosis. We investigate the influence of polymorphisms in the genes encoding toll-like receptor 2 (TLR2) and 4 (TLR4) and endothelial adhesion molecules on polycystic ovary syndrome (PCOS) and its interaction with obesity. Ten single nucleotide polymorphisms were genotyped in 305 women with PCOS and 166 non-hyperandrogenic control women. In obese women, TLR2 S450S and ICAM1 K469E polymorphisms differently influenced metabolic variables and PCOS, respectively. Irrespective of PCOS, variant alleles of TLR2 S450S increased triglycerides, fasting insulin levels, and insulin resistance in obese women. TLR2 S450S interacted with obesity and PCOS on androstenedione levels, mutant alleles were associated with increased androstenedione concentrations in all women, with the exception of obese patients with PCOS (P=0.034). Regarding ICAM1 K469E, homozygosis for K469 alleles was more frequent in PCOS, but only in obese women (P=0.014). K469 alleles were also related to increased body mass index (P=0.017) and diastolic blood pressure (P=0.034). Moreover, ICAM1 K469E interacted with obesity and PCOS on serum triglyceride levels (P=0.019) and with PCOS on serum sex hormone-binding globulin concentrations (P=0.006). In conclusion, TLR2 S450S and ICAM1 K469E polymorphisms may be associated with PCOS and metabolic comorbidities in obese women.

  10. 运动对大鼠心肌ICAM-1表达与超微结构的影响%Influences of exercise on myocardic ICAM-1 expression and cardiac ultrastructure in rats

    Institute of Scientific and Technical Information of China (English)

    毛宗珍; 李恩荆; 葛新发

    2004-01-01

    通过不同负荷大鼠运动模型的建立,观察大鼠心肌超微结构及ICAM-1表达.结果发现:一般训练组心肌呈与有氧代谢相适应的生理性肥大,心肌细胞ICAM-1表达为阴性;过度负荷组呈现病理性改变,心肌细胞ICAM-1表达为阳性;且大鼠心肌ICAM-1表达率与心脏肥大程度呈正相关.提示心肌ICAM-1表达可作为过度训练的诊断指标;ICAM-1可作为心脏生理性肥大和病理性肥大的鉴别指标.

  11. 粘附分子在复发性口腔溃疡的发病机制中作用的探讨%Expression of vascular cell adhesion molecule-1 in recurrent oral ulceration

    Institute of Scientific and Technical Information of China (English)

    孙睿; 董玙; 晁海英; 孙晓震

    2003-01-01

    目的:探讨可溶性血管内皮细胞粘附分子(sVCAM-1)、可溶性细胞间粘附分子(sICAM-1)在复发性口腔溃疡(recurrent oral ulceration,ROU)发病机制中的作用.方法:采用双抗体夹心酶联免疫吸附实验法检测血清中的sVCAM-1、sICAM-1浓度.结果:ROU患者的sVCAM-1浓度高于健康对照组,差异有显著性.ROU患者的sICAM-1浓度与健康对照组相比无显著性差异.sVCAM-1、sICAM-1两者浓度在活动期与静止期差异无显著性.结论:sVCAM 1在复发性口腔溃疡发病机制中可能有重要意义.

  12. Evaluation of ICAM-1 and VCAM-1 Gene Polymorphisms in Patients with Periodontal Disease.

    Science.gov (United States)

    Wang, Li; Li, Xiao-Hong; Ning, Wan-Chen

    2016-01-01

    BACKGROUND We aimed to investigate the potential genetic relationships between the polymorphisms of gene rs5498 ICAM-1 and rs1041163 VCAM-1 and chronic periodontitis in a Chinese population within Heilongjiang. MATERIAL AND METHODS Genomic DNA was extracted from oral mucosa cells of 584 periodontal patients and 182 healthy individuals. Genotyping of the rs5498 ICAM-1 and rs1041163 VCAM-1 gene polymorphisms was performed with the Multiplex SNaPshot technique. RESULTS Statistically significant associations were identified between the chronic periodontal patients and the controls in the gene polymorphisms of rs5498 ICAM-1 (P=0.007) and rs1041163 VCAM-1 (P=0.029). The distribution of rs5498 (P=0.029) and rs1041163 (P=0.049) differed significantly across the mild, moderate, and severe groups of periodontitis. CONCLUSIONS Our findings indicate that ICAM-1 rs5498 and VCAM-1 rs1041163 polymorphisms contribute to chronic periodontitis, and ICAM-1 rs5498 and VCAM-1 rs1041163 gene polymorphisms might be associated with periodontitis severity in the Heilongjiang Chinese population. Further studies should be conducted to determine whether these polymorphisms could be used as biomarkers of periodontitis. PMID:27391418

  13. Functional Implication of the Hydrolysis of Platelet Endothelial Cell Adhesion Molecule 1 (CD31) by Gingipains of Porphyromonas gingivalis for the Pathology of Periodontal Disease

    OpenAIRE

    Yun, Peter L. W.; DeCarlo, Arthur A.; Chapple, Cheryl C.; Hunter, Neil

    2005-01-01

    Periodontitis is a response of highly vascularized tissues to the adjacent microflora of dental plaque. Progressive disease has been related to consortia of anaerobic bacteria, with the gram-negative organism Porphyromonas gingivalis particularly implicated. The gingipains, comprising a group of cysteine proteinases and associated hemagglutinin domains, are major virulence determinants of this organism. As vascular expression of leukocyte adhesion molecules is a critical determinant of tissue...

  14. Opiates Upregulate Adhesion Molecule Expression in Brain MicroVascular Endothelial Cells (BMVEC: Implications for Altered Blood Brain Barrier (BBB Permeability

    Directory of Open Access Journals (Sweden)

    Madhavan P.N. Nair

    2006-01-01

    Full Text Available The blood-brain barrier (BBB is an intricate cellular system composed of vascular endothelial cells and perivascular astrocytes that restrict the passage of immunocompetent cells into the central nervous system (CNS. Expression of the adhesion molecules, intercellular adhesion molecule 1 (ICAM-1 and vascular cell adhesion molecule-1 (VCAM-1 on brain microvascular endothelial cells (BMVEC and their interaction with human immunodeficiency virus (HIV-1 viral proteins may help enhance viral adhesion and virus-cell fusion resulting in increased infectivity. Additionally, transmigration through the BBB is facilitated by both endothelial and monocyte/macrophage-derived nitric oxide (NO. Dysregulated production of NO by BMVEC due to opiates and HIV-1 viral protein interactions play a pivotal role in brain endothelial injury, resulting in the irreversible loss of BBB integrity, which may lead to enhanced infiltration of virus-carrying cells across the BBB. Opioids act as co-factors in the neuropathogenesis of HIV-1 by facilitating BBB dysfunction however, no studies have been done to investigate the role of opiates alone or in combination with HIV-1 viral proteins on adhesion molecule expression in BMVEC. We hypothesize that opiates such as heroin and morphine in conjunction with the HIV-1 viral protein gp120 increase the expression of adhesion molecules ICAM-1 and VCAM-1 and these effects are mediated via the modulation of NO. Results show that opiates alone and in synergy with gp120 increase both the genotypic and phenotypic expression of ICAM-1 and VCAM-1 by BMVEC, additionally, these opiate induced effects may be the result of increased NO production. These studies will provide a better understanding of how opiate abuse in conjunction with HIV-1 infection facilitates the breakdown of the BBB and exacerbates the neuropathogenesis of HIV-1. Elucidation of the mechanisms of BBB modulation will provide new therapeutic approaches to maintain BBB integrity

  15. Distribution of ICAM-1-ASO and Its Effect on ICAM-1 Expression%细胞间粘附分子-1反义寡核苷酸在小鼠体内的分布及其作用

    Institute of Scientific and Technical Information of China (English)

    柳祎; 孙宗全

    2005-01-01

    目的探讨细胞间粘附分子-1反义寡核苷酸(ICAM-1-ASO)静脉注射后在小鼠体内的分布及其对心脏组织ICAM-1表达的作用.方法 FITC荧光标记的ICAM-1-ASO(10 mg/kg)经小鼠颈外静脉注射6 h后,应用荧光显微镜观察其在小鼠体内的分布;取心脏组织进行免疫组织化学及半定量RT-PCR检测,观察心脏组织中ICAM-1的表达,研究ICAM-1-ASO对心脏组织ICAM-1表达的作用.结果 ICAM-1-ASO经静脉注射6 h后,在肾脏以及心脏组织中可见较多的颗粒状荧光分布,而在肝、肺、脾组织中仅见少量散在的荧光分布.RT-PCR检测表明ICAM-1-ASO(10 mg/kg)可降低心脏组织中ICAM-1 mRNA水平;但免疫组织化学检测各组间ICAM-1的蛋白水平未显示出显著性差异.结论 ICAM-1-ASO经静脉注射6 h后可以明显抑制心脏组织ICAM-1 mRNA的表达,其作用的理想靶器官是心脏和肾脏.

  16. NADPH oxidase and lipid raft-associated redox signaling are required for PCB153-induced upregulation of cell adhesion molecules in human brain endothelial cells

    International Nuclear Information System (INIS)

    Exposure to persistent organic pollutants, such as polychlorinated biphenyls (PCBs), can lead to chronic inflammation and the development of vascular diseases. Because cell adhesion molecules (CAMs) of the cerebrovascular endothelium regulate infiltration of inflammatory cells into the brain, we have explored the molecular mechanisms by which ortho-substituted polychlorinated biphenyls (PCBs), such as PCB153, can upregulate CAMs in brain endothelial cells. Exposure to PCB153 increased expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), as well as elevated adhesion of leukocytes to brain endothelial cells. These effects were impeded by inhibitors of EGFR, JAKs, or Src activity. In addition, pharmacological inhibition of NADPH oxidase or disruption of lipid rafts by cholesterol depleting agents blocked PCB153-induced phosphorylation of JAK and Src kinases and upregulation of CAMs. In contrast, silencing of caveolin-1 by siRNA interference did not affect upregulation of ICAM-1 and VCAM-1 in brain endothelial cells stimulated by PCB153. Results of the present study indicate that lipid raft-dependent NADPH oxidase/JAK/EGFR signaling mechanisms regulate the expression of CAMs in brain endothelial cells and adhesion of leukocytes to endothelial monolayers. Due to its role in leukocyte infiltration, induction of CAMs may contribute to PCB-induced cerebrovascular disorders and neurotoxic effects in the CNS.

  17. A role for cell adhesion in beryllium-mediated lung disease

    Energy Technology Data Exchange (ETDEWEB)

    Hong-geller, Elizabeth [Los Alamos National Laboratory

    2008-01-01

    Chronic beryllium disease (CBD) is a debilitating lung disorder in which exposure to the lightweight metal beryllium (Be) causes the accumulation of beryllium-specific CD4+ T cells in the lung and formation of noncaseating pulmonary granulomas. Treatment for CBD patients who exhibit progressive pulmonary decline is limited to systemic corticosteroids, which suppress the severe host inflammatory response. Studies in the past several years have begun to highlight cell-cell adhesion interactions in the development of Be hypersensitivity and CBD. In particular, the high binding affinity between intercellular adhesion molecule 1 (I-CAM1) on lung epithelial cells and the {beta}{sub 2} integrin LFA-1 on migrating lymphocytes and macrophages regulates the concerted rolling of immune cells to sites of inflammation in the lung. In this review, we discuss the evidence that implicates cell adhesion processes in onset of Be disease and the potential of cell adhesion as an intervention point for development of novel therapies.

  18. Rolling adhesion of alphaL I domain mutants decorrelated from binding affinity.

    Science.gov (United States)

    Pepper, Lauren R; Hammer, Daniel A; Boder, Eric T

    2006-06-30

    Activated lymphocyte function-associated antigen-1 (LFA-1, alphaLbeta2 integrin) found on leukocytes facilitates firm adhesion to endothelial cell layers by binding to intercellular adhesion molecule-1 (ICAM-1), which is up-regulated on endothelial cells at sites of inflammation. Recent work has shown that LFA-1 in a pre-activation, low-affinity state may also be involved in the initial tethering and rolling phase of the adhesion cascade. The inserted (I) domain of LFA-1 contains the ligand-binding epitope of the molecule, and a conformational change in this region during activation increases ligand affinity. We have displayed wild-type I domain on the surface of yeast and validated expression using I domain specific antibodies and flow cytometry. Surface display of I domain supports yeast rolling on ICAM-1-coated surfaces under shear flow. Expression of a locked open, high-affinity I domain mutant supports firm adhesion of yeast, while yeast displaying intermediate-affinity I domain mutants exhibit a range of rolling phenotypes. We find that rolling behavior for these mutants fails to correlate with ligand binding affinity. These results indicate that unstressed binding affinity is not the only molecular property that determines adhesive behavior under shear flow.

  19. RT-PCR法研究肝星状细胞ICAM-1的表达

    Institute of Scientific and Technical Information of China (English)

    陆伦根; 曹民德; 范建高; 华静; 李继强; 邱德凯; 范竹萍

    1998-01-01

    目的:研究肝星状细胞(HSC)与细胞间粘附分子-1(ICAM-1)表达的关系。方法:用链酶蛋白酶和胶原酶原位灌流,Nycodenz密度梯度离心分别分离正常大鼠及CCl4实验性大鼠肝纤维化模型中的HSC,并进行体外培养,应用免疫组织化学方法和RT-PCR技术分别观察不同培养时期的HSC、正常及造模肝组织中HSC的ICAM-1的表达。结果:正常大鼠新分离的HSC中,ICAM-1不表达;原代培养第7天及传代培养的HSC表达ICAM-1,且随着培养时间的延长ICAM-1表达量逐渐增加。CCl4实验性大鼠肝纤维化模型中,新分离的HSC中即可见ICAM-1表达。结论:体内动物实验和体外细胞培养表明,ICAM-1表达可能与HSC活化、肝脏炎性损伤及肝纤维化的发生有关。

  20. Neutrophil Transmigration Mediated by the Neutrophil-Specific Antigen CD177 Is Influenced by the Endothelial S536N Dimorphism of Platelet Endothelial Cell Adhesion Molecule-1

    OpenAIRE

    Bayat, Behnaz; Werth, Silke; Sachs, Ulrich J. H.; Newman, Debra K.; Newman, Peter J.; Santoso, Sentot

    2010-01-01

    The human neutrophil-specific adhesion molecule CD177 (also known as the NB1 alloantigen) becomes upregulated on the cell surface in a number of inflammatory settings. We recently showed that CD177 functions as a novel heterophilic counterreceptor for the endothelial junctional protein PECAM-1 (CD31), an interaction that is mediated by membrane-proximal PECAM-1 IgD 6, which is known to harbor an S536N single nucleotide polymorphism of two major isoforms V98N536G643 and L98S536R643 and a yet-t...

  1. Gene deletion of P-Selectin and ICAM-1 does not inhibit neutrophil infiltration into peritoneal cavity following cecal ligation-puncture

    Directory of Open Access Journals (Sweden)

    Hess Karen

    2004-07-01

    Full Text Available Abstract Background Neutrophil infiltration is one of the critical cellular components of an inflammatory response during peritonitis. The adhesion molecules, P-selectin and intercellular adhesion molecule (ICAM-1, mediate neutrophil-endothelial cell interactions and the subsequent neutrophil transendothelial migration during the inflammatory response. Despite very strong preclinical data, recent clinical trials failed to show a protective effect of anti-adhesion therapy, suggesting that the length of injury might be a critical factor in neutrophil infiltration. Therefore, the objective of this study was to determine the role of P-selectin and ICAM-1 in neutrophil infiltration into the peritoneal cavity during early and late phases of peritonitis. Methods Peritonitis was induced in both male wild-type and P-selectin/ICAM-1 double deficient (P/I null mice by cecal ligation-puncture (CLP. Peripheral blood and peritoneal lavage were collected at 6 and 24 hours after CLP. The total leukocyte and neutrophil contents were determined, and neutrophils were identified with the aid of in situ immunohistochemical staining. Comparisons between groups were made by applying ANOVA and student t-test analysis. Results CLP induced a severe inflammatory response associated with a significant leukopenia in both wild-type and P/I null mice. Additionally, CLP caused a significant neutrophil infiltration into the peritoneal cavity that was detected in both groups of mice. However, neutrophil infiltration in the P/I null mice at 6 hours of CLP was significantly lower than the corresponding wild-type mice, which reached a similar magnitude at 24 hours of CLP. In contrast, in peritonitis induced by intraperitoneal inoculation of 2% glycogen, no significant difference in neutrophil infiltration was observed between the P/I null and wild-type mice at 6 hours of peritonitis. Conclusions The data suggest that alternative adhesion pathway(s independent of P-selectin and ICAM

  2. CXC-chemokine regulation and neutrophil trafficking in hepatic ischemia-reperfusion injury in P-selectin/ICAM-1 deficient mice

    Directory of Open Access Journals (Sweden)

    Crockett Elahé T

    2007-05-01

    Full Text Available Abstract Background Neutrophil adhesion and migration are critical in hepatic ischemia and reperfusion injury (I/R. P-selectin and the intercellular adhesion molecule (ICAM-1 can mediate neutrophil-endothelial cell interactions, neutrophil migration, and the interactions of neutrophils with hepatocytes in the liver. Despite very strong preclinical data, recent clinical trials failed to show a protective effect of anti-adhesion therapy in reperfusion injury, indicating that the length of injury might be a critical factor in neutrophil infiltration. Therefore, the aim of this study was to assess the role of P-selectin and ICAM-1 in neutrophil infiltration and liver injury during early and late phases of liver I/R. Methods Adult male wild-type and P-selectin/ICAM-1-deficient (P/I null mice underwent 90 minutes of partial liver ischemia followed by various periods of reperfusion (6, 15 h, and a survival study. Liver injury was assessed by plasma level of alanine aminotransferase (ALT and histopathology. The plasma cytokines, TNF-α, IL-6, MIP-2 and KC, were measured by ELISA. Results Reperfusion caused significant hepatocellular injury in both wild-type and P/I null mice as was determined by plasma ALT levels and liver histopathology. The injury was associated with a marked neutrophil infiltration into the ischemic livers of both wild-type and P/I null mice. Although the levels of ALT and neutrophil infiltration were slightly lower in the P/I null mice compared with the wild-type mice the differences were not statistically significant. The plasma cytokine data of TNF-α and IL-6 followed a similar pattern to ALT data, and no significant difference was found between the wild-type and P/I null groups. In contrast, a significant difference in KC and MIP-2 chemokine levels was observed between the wild-type and P/I null mice. Additionally, the survival study showed a trend towards increased survival in the P/I null group. Conclusion While ICAM-1 and P

  3. Syndrome differentiation in traditional Chinese medicine and E-cadherin/ICAM-1 gene protein expression in gastric carcinoma

    Institute of Scientific and Technical Information of China (English)

    2007-01-01

    AIM: To explore the syndrome differentiation in traditional Chinese medicine (TCM) and gene protein expression in gastric carcinoma METHODS: Preoperative data of gastric cancer cases were collected from the General Surgery Department and classified according to the criteria for syndrome differentiation in TCM. E-cadherin (E-cad) and ICAM-1 gene protein expressions were detected in postoperative specimens from these cases by the immunohistochemical EnVision two-step method.RESULTS: The E-cad positive expression rate was 90% in 100 cases of gastric carcinoma. The difference in E-cad expression was significant between thedifferent syndrome differentiation types in TCM (P <0.01). Further group-group comparison showed that there was a significant difference in E-cad expression between the stagnation of phlegm-damp type and the deficiency in both qi and blood and the deficiency-cold of stomach and spleen types, where E-cad expression was high. There was no significant difference between the internal obstruction of stagnant toxin type and the in-coordination between liver and stomach type, where E-cad expression was relatively low. The ICAM-1 positive expression rate was 58%, and there was no statistically significant difference between the two groups (χ2= 8.999,P > 0.05).CONCLUSION: E-cad expression is relatively low in the internal obstruction of stagnant toxin type and the incoordination between liver and stomach type, where tumor development and metastasis may be associated with low E-cad expression, or with low homogeneous adhesiveness between tumor cells.

  4. Expression of adhesion molecules, chemokines and matrix metallo- proteinases (MMPs) in viable and degenerating stage of Taenia solium metacestode in swine neurocysticercosis.

    Science.gov (United States)

    Singh, Satyendra K; Singh, Aloukick K; Prasad, Kashi N; Singh, Amrita; Singh, Avinash; Rai, Ravi P; Tripathi, Mukesh; Gupta, Rakesh K; Husain, Nuzhat

    2015-11-30

    Neurocysticercosis (NCC) is a parasitic infection of central nervous system (CNS). Expression of adhesion molecules, chemokines and matrix metalloproteinases (MMPs) were investigated on brain tissues surrounding viable (n=15) and degenerating cysticerci (n=15) of Taenia solium in swine by real-time RT-PCR and ELISA. Gelatin gel zymography was performed for MMPs activity. ICAM-1 (intercellular adhesion molecule-1), E-selectin, MIP-1α (macrophage inflammatory protein-1α), Eotaxin-1 and RANTES (regulated on activation, normal T cell expressed and secreted) were associated with degenerating cysticerci (cysts). However, VCAM-1 (vascular cell adhesion molecule-1), MCP-1 (monocyte chemotactic protein-1), MMP-2 and MMP-9 were associated with both viable and degenerating cysts. In conclusion, viable and degenerating cysticerci have different immune molecule profiles and role of these molecules in disease pathogenesis needs to be investigated. PMID:26412140

  5. Expression of adhesion molecules, chemokines and matrix metallo- proteinases (MMPs) in viable and degenerating stage of Taenia solium metacestode in swine neurocysticercosis.

    Science.gov (United States)

    Singh, Satyendra K; Singh, Aloukick K; Prasad, Kashi N; Singh, Amrita; Singh, Avinash; Rai, Ravi P; Tripathi, Mukesh; Gupta, Rakesh K; Husain, Nuzhat

    2015-11-30

    Neurocysticercosis (NCC) is a parasitic infection of central nervous system (CNS). Expression of adhesion molecules, chemokines and matrix metalloproteinases (MMPs) were investigated on brain tissues surrounding viable (n=15) and degenerating cysticerci (n=15) of Taenia solium in swine by real-time RT-PCR and ELISA. Gelatin gel zymography was performed for MMPs activity. ICAM-1 (intercellular adhesion molecule-1), E-selectin, MIP-1α (macrophage inflammatory protein-1α), Eotaxin-1 and RANTES (regulated on activation, normal T cell expressed and secreted) were associated with degenerating cysticerci (cysts). However, VCAM-1 (vascular cell adhesion molecule-1), MCP-1 (monocyte chemotactic protein-1), MMP-2 and MMP-9 were associated with both viable and degenerating cysts. In conclusion, viable and degenerating cysticerci have different immune molecule profiles and role of these molecules in disease pathogenesis needs to be investigated.

  6. Pentosan polysulfate treatment ameliorates motor function with increased serum soluble vascular cell adhesion molecule-1 in HTLV-1-associated neurologic disease.

    Science.gov (United States)

    Nakamura, Tatsufumi; Satoh, Katsuya; Fukuda, Taku; Kinoshita, Ikuo; Nishiura, Yoshihiro; Nagasato, Kunihiko; Yamauchi, Atsushi; Kataoka, Yasufumi; Nakamura, Tadahiro; Sasaki, Hitoshi; Kumagai, Kenji; Niwa, Masami; Noguchi, Mitsuru; Nakamura, Hideki; Nishida, Noriyuki; Kawakami, Atsushi

    2014-06-01

    The main therapeutic strategy against human T lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) characterized by lower extremity motor dysfunction is immunomodulatory treatment, with drugs such as corticosteroid hormone and interferon-α, at present. However, there are many issues in long-term treatment with these drugs, such as insufficient effects and various side effects. We now urgently need to develop other therapeutic strategies. The heparinoid, pentosan polysulfate sodium (PPS), has been safely used in Europe for the past 50 years as a thrombosis prophylaxis and for the treatment of phlebitis. We conducted a clinical trial to test the effect of subcutaneous administration of PPS in 12 patients with HAM/TSP in an open-labeled design. There was a marked improvement in lower extremity motor function, based on reduced spasticity, such as a reduced time required for walking 10 m and descending a flight of stairs. There were no significant changes in HTLV-I proviral copy numbers in peripheral blood contrary to the inhibitory effect of PPS in vitro for intercellular spread of HTLV-I. However, serum soluble vascular cell adhesion molecule (sVCAM)-1 was significantly increased without significant changes of serum level of chemokines (CXCL10 and CCL2). There was a positive correlation between increased sVCAM-1and reduced time required for walking 10 m. PPS might induce neurological improvement by inhibition of chronic inflammation in the spinal cord, through blocking the adhesion cascade by increasing serum sVCAM-1, in addition to rheological improvement of the microcirculation. PPS has the potential to be a new therapeutic tool for HAM/TSP.

  7. Neutrophil transmigration mediated by the neutrophil-specific antigen CD177 is influenced by the endothelial S536N dimorphism of platelet endothelial cell adhesion molecule-1.

    Science.gov (United States)

    Bayat, Behnaz; Werth, Silke; Sachs, Ulrich J H; Newman, Debra K; Newman, Peter J; Santoso, Sentot

    2010-04-01

    The human neutrophil-specific adhesion molecule CD177 (also known as the NB1 alloantigen) becomes upregulated on the cell surface in a number of inflammatory settings. We recently showed that CD177 functions as a novel heterophilic counterreceptor for the endothelial junctional protein PECAM-1 (CD31), an interaction that is mediated by membrane-proximal PECAM-1 IgD 6, which is known to harbor an S(536)N single nucleotide polymorphism of two major isoforms V(98)N(536)G(643) and L(98)S(536)R(643) and a yet-to-be-determined region on CD177. In vitro transendothelial migration experiments revealed that CD177(+) neutrophils migrated significantly faster through HUVECs expressing the LSR, compared with the VNG, allelic variant of PECAM-1 and that this correlated with the decreased ability of anti-PECAM-1 Ab of ITIM tyrosine phosphorylation in HUVECs expressing the LSR allelic variant relative to the VNG allelic variant. Moreover, engagement of PECAM-1 with rCD177-Fc (to mimic heterophilic CD177 binding) suppressed Ab-induced tyrosine phosphorylation to a greater extent in cells expressing the LSR isoform compared with the VNG isoform, with a corresponding increased higher level of beta-catenin phosphorylation. These data suggest that heterophilic PECAM-1/CD177 interactions affect the phosphorylation state of PECAM-1 and endothelial cell junctional integrity in such a way as to facilitate neutrophil transmigration in a previously unrecognized allele-specific manner. PMID:20194726

  8. Association between Arsenic Exposure from Drinking Water and Plasma Levels of Soluble Cell Adhesion Molecules

    Science.gov (United States)

    Chen, Yu; Santella, Regina M.; Kibriya, Muhammad G.; Wang, Qiao; Kappil, Maya; Verret, Wendy J.; Graziano, Joseph H.; Ahsan, Habibul

    2007-01-01

    Background Epidemiologic studies of cardiovascular disease risk factors and appropriate biomarkers in populations exposed to a wide range of arsenic levels are a public health research priority. Objective We investigated the relationship between inorganic arsenic exposure from drinking water and plasma levels of soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular adhesion molecule-1 (sVCAM-1), both markers of endothelial dysfunction and vascular inflammation, in an arsenic-exposed population in Araihazar, Bangladesh. Methods The study participants included 115 individuals with arsenic-related skin lesions participating in a 2 × 2 randomized, placebo-controlled, double-blind trial of vitamin E and selenium supplementation. Arsenic exposure status and plasma levels of sICAM-1 and sVCAM-1 were assessed at baseline and after 6 months of follow-up. Results Baseline well arsenic, a long-term measure of arsenic exposure, was positively associated with baseline levels of both sICAM-1 and sVCAM-1 and with changes in the two markers over time. At baseline, for every 1-μg/L increase in well arsenic there was an increase of 0.10 ng/mL [95% confidence interval (CI), 0.00–0.20] and 0.33 ng/mL (95% CI, 0.15–0.51) in plasma sICAM-1 and sVCAM-1, respectively. Every 1-μg/L increase in well arsenic was associated with a rise of 0.11 ng/mL (95% CI, 0.01–0.22) and 0.17 ng/mL (95% CI, 0.00–0.35) in sICAM-1 and sVCAM-1 from baseline to follow-up, respectively, in spite of recent changes in urinary arsenic as well as vitamin E and selenium supplementation during the study period. Conclusions The findings indicate an effect of chronic arsenic exposure from drinking water on vascular inflammation that persists over time and also suggest a potential mechanism underlying the association between arsenic exposure and cardiovascular disease. PMID:17938729

  9. Construction of ICAM-1-GFP and Its Binding with Molt-4 Cells%ICAM-1-GFP的构建及其与Molt-4细胞的结合

    Institute of Scientific and Technical Information of China (English)

    陈卫华; 达万明; 高春记

    2009-01-01

    本研究构建人细胞间黏附分子1(ICAM-1)全长基因的真核表达载体pEGFP-Cl-ICAM-1,转染中国仓鼠卵巢细胞(CHO-K1)细胞株,并检测其在CHO细胞中的表达及与Molt-4细胞的结合.采用RT-PCR法从健康人外周血中分离单个核细胞,钓取ICAM-1全长基因(1622 bp),与pMD18-T载体连接做全自动序列测定.将测序正确的克隆质粒pMD18-T-ICAM-1和表达载体pEGFP-C1分别用HindⅢ和Ⅰ进行双酶切,应用基因重组技术构建ICAM-1全长基因真核表达载体pEGFP-Cl-ICAM-1,质粒经Hind Ⅲ和Sacll双酶切和PCR电泳鉴定后,采用脂质体转染法转染CHO细胞,并进行G418筛选.用RT-PCR、流式细胞术和荧光显微术检测ICAM-1-GFP的表达及亚细胞的定位,用检测ICAM-1-GFP/CHO细胞与Molt-4细胞的结合能力评价ICAM-1-GFP融合蛋白的功能.结果表明:重组质粒经限制性酶切鉴定得到与ICAM-1全长基因长度一致(1622 bp)的酶切产物;测序分析证实,PCR产物与GenBank上登录的ICAM-1基因(NM_000201)序列完全一致,表明成功地完成了ICAM-1的扩增和表达载体的构建;荧光显微镜下可见转染的CHO细胞有绿色荧光蛋白的表达,表达的融合蛋白较均匀地分布于整个细胞:FACS检测ICAM-1-GFP的荧光转染率为(13±5.5)%,表明ICAM-1-GFP基因进入到CHO细胞并获得了有效表达,成功构建了ICAM-1-GFP/CHO细胞,并且ICAM-1-GFP/CHO细胞能够结合PMA处理的Molt-4细胞.结论:成功构建了ICAM-1-GFP真核表达载体,构建的ICAM-1-GFP真核表达载体在CHO细胞内稳定表达,ICAM-1-GFP/CHO细胞能与Molt-4细胞结合.这为进一步研究ICAM-1分子的功能打下基础.

  10. Potential of mZD7349-conjugated PLGA nanoparticles for selective targeting of vascular cell-adhesion molecule-1 in inflamed endothelium.

    Science.gov (United States)

    Imanparast, Fatemeh; Paknejad, Maliheh; Faramarzi, Mohammad Ali; Kobarfard, Farzad; Amani, Amir; Doosti, Mahmood

    2016-07-01

    Early diagnosis and restoring normal function of dysfunctional endothelium is an attractive strategy for prevention of inflammatory diseases such as atherosclerosis. Inhibition of cell adhesion in the process of atherosclerosis plaque formation, mediated by peptide antagonists of very late antigen-4 (VLA-4) has already been developed and evaluated both in vitro and in vivo. In this study, for the first time, modified ZD7349 (mZD7349) peptide, as an antagonist for VLA-4, was used for targeting fluorescein isothiocyanate-loaded poly (DL-lactic-co-glycolic acid) nanoparticles (FITC-PLGA NPs). Rate of binding and internalization of mZD7349-NPs to activated human umbilical vein endothelial cells (HUVECs) were compared with that of untargeted. Effects of temperature reduction and clathrin-mediated endocytosis inhibitor (0.45M sucrose) were also studied on the binding and internalization of mZD7349-NPs and NPs. Results showed that binding of the conjugated NPs could be significantly blocked by pre-incubating cells with the free peptide, suggesting that the binding of NPs is mediated by attaching the surface peptide to VCAM-1 on HUVECs. Also, conjugated FITC-loaded NPs were shown to be rapidly endocytosized to a greater extent than the unconjugated ones. The binding and internalization of mZD7349-NPs and NPs were slowed down at low temperature and in the presence of sucrose with greater reductions for mZD7349-NPs. To conclude, the peptide-NPs targeting the VCAM-1 is suggested as a theranostic carrier for lesions upregulating VCAM-1. PMID:27105996

  11. s-ICAM-1 and s-VCAM-1 in healthy men are strongly associated with traits of the metabolic syndrome, becoming evident in the postprandial response to a lipid-rich meal

    Directory of Open Access Journals (Sweden)

    Nothnagel Michael

    2008-09-01

    Full Text Available Abstract Background The importance of the postprandial state for the early stages of atherogenesis is increasingly acknowledged. We conducted assessment of association between postprandial triglycerides, insulin and glucose after ingestion of a standardized lipid-rich test meal, and soluble cellular adhesion molecules (sCAM in young healthy subjects. Methods Metabolic parameters and sICAM-1, sVCAM-1 and E-selectin were measured before and hourly until 6 hours after ingestion of a lipid-rich meal in 30 healthy young men with fasting triglycerides 260 mg/dl. Levels of CAM were compared in HR and NR, and correlation with postprandial triglyceride, insulin and glucose response was assessed. Results Fasting sICAM-1 and sVCAM-1 levels were significantly higher in HR as compared to NR (p = 0.046, p = 0.03. For sE-selectin there was such a trend (p = 0.05. There was a strong positive and independent correlation between sICAM-1 and postprandial insulin maxima (r = 0.70, p Conclusion This independent association of postprandial triglycerides with sICAM-1 may indicate a particular impact of postprandial lipid metabolism on endothelial reaction.

  12. The Expression of TNF-α and ICAM-1 in Lesions of Lichen Planus and Its Implication

    Institute of Scientific and Technical Information of China (English)

    CHEN Xue; LIU Zhixiang; YUE Qing; LIU Houjun; WU Yan; LI Jiawen

    2007-01-01

    In order to investigate the role of TNF-α and ICAM-1 in the pathogenesis of lichen planus, immunohistechemistty was used to detect the expression of TNF-α and ICAM-1 in skin le- sions of the patients with lichen planus and skin tissues of normal subjects. The results showed that positive rates of TNF-α and ICAM-1 expressions in lichen planus were significantly higher than those in normal skins (both P<0.05). Meanwhile, there was a obvious correlation between the in- crease of TNF-α and that of ICAM-1 in lichen planus. The expression of TNF-α and ICAM-1 might play an important role in the development of lichen planus.

  13. Ambient pollutants, polymorphisms associated with microRNA processing and adhesion molecules: the Normative Aging Study

    Directory of Open Access Journals (Sweden)

    Vokonas Pantel S

    2011-05-01

    Full Text Available Abstract Background Particulate air pollution has been associated with cardiovascular morbidity and mortality, but it remains unclear which time windows and pollutant sources are most critical. MicroRNA (miRNA is thought to be involved in cardiovascular regulation. However, little is known about whether polymorphisms in genes that process microRNAs influence response to pollutant exposure. We hypothesized that averaging times longer than routinely measured one or two day moving averages are associated with higher soluble intercellular adhesion molecule-1 (sICAM-1 and vascular cell adhesion molecule-1 (sVCAM-1 levels, and that stationary and mobile sources contribute differently to these effects. We also investigated whether single nucleotide polymorphisms (SNPs in miRNA-processing genes modify these associations. Methods sICAM-1 and sVCAM-1 were measured from 1999-2008 and matched to air pollution monitoring for fine particulate matter (PM2.5 black carbon, and sulfates (SO42-. We selected 17 SNPs in five miRNA-processing genes. Mixed-effects models were used to assess effects of pollutants, SNPs, and interactions under recessive inheritance models using repeated measures. Results 723 participants with 1652 observations and 1-5 visits were included in our analyses for black carbon and PM2.5. Sulfate data was available for 672 participants with 1390 observations. An interquartile range change in seven day moving average of PM2.5 (4.27 μg/m3 was associated with 3.1% (95%CI: 1.6, 4.6 and 2.5% (95%CI: 0.6, 4.5 higher sICAM-1 and sVCAM-1. Interquartile range changes in sulfates (1.39 μg/m3 were associated with 1.4% higher (95%CI: 0.04, 2.7 and 1.6% (95%CI: -0.4, 3.7 higher sICAM-1 and sVCAM-1 respectively. No significant associations were observed for black carbon. In interaction models with PM2.5, both sICAM-1 and sVCAM-1 levels were lower in rs1062923 homozygous carriers. These interactions remained significant after multiple comparisons

  14. Effect of PIP3 on Adhesion Molecules and Adhesion of THP-1 Monocytes to HUVEC Treated with High Glucose

    Directory of Open Access Journals (Sweden)

    Prasenjit Manna

    2014-04-01

    Full Text Available Background: Phosphatidylinositol-3,4,5-triphosphate (PIP3, a well-known lipid second messenger, plays a key role in insulin signaling and glucose homeostasis. Using human umbilical vein endothelial cells (HUVEC and THP-1 monocytes, we tested the hypothesis that PIP3 can downregulate adhesion molecules and monocyte adhesion to endothelial cells. Methods: HUVEC and monocytes were exposed to high glucose (HG, 25 mM, 20 h with or without PIP3 (0-20 nM, or PIT-1 (25 µM, an inhibitor of PIP3. Results: Both HG and PIT-1 caused a decrease in cellular PIP3 in monocytes and HUVEC compared to controls. Treatment with PIT-1 and HG also increased the ICAM-1 (intercellular adhesion molecule 1 total protein expression as well as its surface expression in HUVEC, CD11a (a subunit of lymphocyte function-associated antigen 1, LFA-1 total protein expression as well as its surface expression in monocytes, and adhesion of monocytes to HUVEC. Exogenous PIP3 supplementation restored the intracellular PIP3 concentrations, downregulated the expression of adhesion molecules, and reduced the adhesion of monocytes to HUVEC treated with HG. Conclusion: This study reports that a decrease in cellular PIP3 is associated with increased expression of adhesion molecules and monocyte-endothelial cell adhesion, and may play a role in the endothelial dysfunction associated with diabetes.

  15. Palmitate-induced inflammatory pathways in human adipose microvascular endothelial cells promote monocyte adhesion and impair insulin transcytosis.

    Science.gov (United States)

    Pillon, Nicolas J; Azizi, Paymon M; Li, Yujin E; Liu, Jun; Wang, Changsen; Chan, Kenny L; Hopperton, Kathryn E; Bazinet, Richard P; Heit, Bryan; Bilan, Philip J; Lee, Warren L; Klip, Amira

    2015-07-01

    Obesity is associated with inflammation and immune cell recruitment to adipose tissue, muscle and intima of atherosclerotic blood vessels. Obesity and hyperlipidemia are also associated with tissue insulin resistance and can compromise insulin delivery to muscle. The muscle/fat microvascular endothelium mediates insulin delivery and facilitates monocyte transmigration, yet its contribution to the consequences of hyperlipidemia is poorly understood. Using primary endothelial cells from human adipose tissue microvasculature (HAMEC), we investigated the effects of physiological levels of fatty acids on endothelial inflammation and function. Expression of cytokines and adhesion molecules was measured by RT-qPCR. Signaling pathways were evaluated by pharmacological manipulation and immunoblotting. Surface expression of adhesion molecules was determined by immunohistochemistry. THP1 monocyte interaction with HAMEC was measured by cell adhesion and migration across transwells. Insulin transcytosis was measured by total internal reflection fluorescence microscopy. Palmitate, but not palmitoleate, elevated the expression of IL-6, IL-8, TLR2 (Toll-like receptor 2), and intercellular adhesion molecule 1 (ICAM-1). HAMEC had markedly low fatty acid uptake and oxidation, and CD36 inhibition did not reverse the palmitate-induced expression of adhesion molecules, suggesting that inflammation did not arise from palmitate uptake/metabolism. Instead, inhibition of TLR4 to NF-κB signaling blunted palmitate-induced ICAM-1 expression. Importantly, palmitate-induced surface expression of ICAM-1 promoted monocyte binding and transmigration. Conversely, palmitate reduced insulin transcytosis, an effect reversed by TLR4 inhibition. In summary, palmitate activates inflammatory pathways in primary microvascular endothelial cells, impairing insulin transport and increasing monocyte transmigration. This behavior may contribute in vivo to reduced tissue insulin action and enhanced tissue

  16. Fu dragon antithrombotic pill on cerebral ischemia reperfusion injury in rat tissue expression of ICAM -1%蝮龙抗栓丸对脑缺血再灌注损伤大鼠脑组织ICAM-1表达的影响

    Institute of Scientific and Technical Information of China (English)

    宋慧峰

    2015-01-01

    目的:观察蝮龙抗栓丸对脑缺血再灌注损伤大鼠脑组织中细胞间黏附因子-1(ICAM-1)含量的影响。方法:利用完全随机法将75只SD大鼠分为:假手术组(15只)、模型组(15只)、治疗I组(15只)、治疗II组(15只)、对照治疗组(15只),予以治疗I组蝮龙抗栓丸0.65mg/g、治疗II组蝮龙抗栓丸1.29mg/g、对照治疗组银杏叶软胶囊0.13mg/g,灌胃1次/天,共计7天。末次灌胃后应用线栓法制备脑缺血再灌注大鼠模型,采用ELISA方法测定各组大鼠脑组织中ICAM-1含量的变化。结果:与模型组比较,各治疗组大鼠脑组织ICAM-1含量比模型组降低(P<0.05)。结论:蝮龙抗栓丸能明显改善大鼠脑缺血再灌注损伤,其机制与降低脑缺血区域中ICAM-1含量有关。%Objective Fu dragon antithrombotic pill on cerebral ischemia reperfusion injury in rat tissues intercellular adhesion factor 1 (ICAM - 1) content.Methods With completely random method, 75 SD rats can be divided into: the control group (15), model group (15), treatment group I (15), treatment group II (15), contrast the treatment group (15), the treatment group I Fu dragon antithrombotic pill 0.65 mg/g, treatment group II Fu dragon antithrombotic pill 1.29 mg/g, contrast treatment group ginkgo biloba soft capsule 0.13 mg/g, lavage 1 time/day, a total of 7 days. After lavage application line plug at the end of the preparation of cerebral ischemia reperfusion model in rats, using ELISA method in the determination of each group rats had changes in concentrations of ICAM - 1.Results Compared with model group, content of ICAM - 1 in each treatment group rats had lower than model group (p < 0.05).Conclusions Fu dragon antithrombotic pill has obvious improvement in ischemia reperfusion injury in rats and its mechanism and reduce ICAM - 1 content in the area of cerebral ischemia.

  17. The investigation of serum procalcitonin,hs-CRP and ICAM-1 in the diagnosis of the neonatal infection%PCT,hs-CRP与ICAM-1在新生儿感染诊断价值的探讨

    Institute of Scientific and Technical Information of China (English)

    吴达党

    2011-01-01

    目的 评价血清降钙素原(PCT),超敏C反应蛋白(hs-CRP)和淋巴细胞黏附因子-1(Intercellularadhesionmolecule1,ICAM-1)的检测在新生儿感染的临床诊断价值.方法 采用ELISA法检测PCT和ICAM-1,速率散射比浊法检测hs-CRP.结果 中、重型新生儿感染组血液中PCT,hS-CRP与ICAM-1浓度明显高于对照组和轻型感染组,差异具有统计学意义(P<0.01); ICAM-1诊断细菌感染的敏感度为81.5%,特异度为85.7%,PCT诊断细菌感染的敏感度为96.3%,特异度为92.9%,感染组ICAM-1、PCT与hs-CRP呈正相关.结论 PCT对于严重感染性疾病的诊断较ICAM-1敏感,联合PCT,hs-CRP与ICAM-1测定能够更早更灵敏地诊断新生儿感染.

  18. MCP-1对培养的人肾小球内皮细胞表达ICAM-1的影响%Effects of MCP-1 on expression of ICAM-1 in cultured humanglomerular endothelial cell

    Institute of Scientific and Technical Information of China (English)

    丁涵露; 朱妙珍; 张建国; 罗向东; 梁光萍

    2001-01-01

    目的研究单核细胞趋化蛋白-1(MCP-1)对培养的人肾小球内皮细胞(HUGEC)表达细胞间粘附分子-1(ICAM-1)的影响.方法采用细胞ELISA法. 结果①培养的HUGEC表面有少量ICAM-1表达,在10 ng/mL MCP-1刺激后ICAM-1表达量增多(P<0.05),6 h即有ICAM-1表达增强,12 h达高峰,不同浓度的MCP-1(10、20、40 ng/mL)刺激HUGEC18 h后,ICAM-1表达与对照组比较差异显著(P<0.01);②加入抗MCP-1抗体后,ICAM-1表达量下降,与对照组比较无差异(P>0.05). 结论 MCP-1可刺激HUGEC表达ICAM-1增加.

  19. Changes of Level of Serum ICAM-1 and its Clinical Significance in Patients with Acute Organic Phosphorus Pesticide Poisoning%急性有机磷农药中毒患者ICAM-1的检测及意义

    Institute of Scientific and Technical Information of China (English)

    关永东; 雷间红; 邓素贞; 陈洁文

    2009-01-01

    目的 探讨急性有机磷农药中毒(AOPP)患者血清细胞间粘附分子-1(ICAM-1)的水平变化及临床意义.方法 采用ELISA法检测68例AOPP患者第1天、第3天、第5天和恢复期(12~14 d)及64例正常健康体检者血清ICAM-1的水平变化.结果 AOPP在第1天的ICAM-1含量最高,与正常对照组比较差异有统计学意义(P0.05);AOPP患者在住院5 d内ICAM-1:轻度组与中度组比较差异有统计学意义(P0.05),compared with control group.Within the first 5 days of the treatment,serum ICAM-1 level were dramatically different between slight group,moderate group and severe group (P<0.05).Serum ICAM-1 level was positively correlated with the severity of AOPP poisoning.Conclusion ICAM-1 was involved in the pathogenesis of AOPP poisoning,and assiociated with the course of AOPP poisoning.

  20. Study on ICAM-1 expression of HepG2 induced by cytokines%细胞因子诱导HepG2细胞ICAM-1表达的研究

    Institute of Scientific and Technical Information of China (English)

    张绪清; 张; 瑞; 顾长海; 王宇明

    2001-01-01

    目的研究IFN-γ、TNF-α和IL-1对HepG2细胞细胞间粘附分子-1(ICAM-1)表达的影响.方法用IFN-γ、TNF-α和IL-1在体外诱导HepG2细胞表达ICAM-1,并用细胞ELISA检测HepG2细胞ICAM-1表达水平.结果未经刺激的HepG2细胞ICAM-1表达水平很低.TNF-α、IL-1、IFN-γ刺激后,HepG2细胞ICAM-1表达均明显增强,其表达水平与细胞因子浓度呈一定的剂量依赖关系;随着细胞因子刺激时间的延长,HepG2细胞ICAM-1表达也逐渐增多.结论 IFN-γ、TNF-α和IL-1等细胞因子能诱导体外培养HepG2细胞ICAM-1增强表达.

  1. LFA-1与配体ICAM-1黏附分子功能的研究进展%An Update on β2 Integrin LFA-1 and Ligand ICAM-1 Signaling Review

    Institute of Scientific and Technical Information of China (English)

    李猛; 高春记

    2008-01-01

    LFA-1和ICAM-1介导的跨膜双向信号传递在淋巴细胞渗出、活化、黏附、免疫监视、免疫突触形成中都起到重要作用.LFA-1与ICAM-1转导信号依赖于两者之间结合能力的变化.LFA-1对ICAM-1结合能力的调节是一动态过程,LFA-1的亲和力和亲合力变化是两种主要调节方式.LFA-1亚单位的磷酸化、细胞骨架蛋白talin1在LFA-1和ICAM-1信号调节中起重要作用.LFA-1和ICAM-1还可提供协同刺激信号促进淋巴细胞活化、增殖和分化.本文就LFA-1结合能力的调节、LFA-1亚单位的磷酸化调节、talin1在LFA-1和ICAM-1信号转导中的作用、LFA-1与ICAM-1的协同刺激信号进行了综述.

  2. ICAM-1 targeted catalase encapsulated PLGA-b-PEG nanoparticles against vascular oxidative stress.

    Science.gov (United States)

    Sari, Ece; Tunc-Sarisozen, Yeliz; Mutlu, Hulya; Shahbazi, Reza; Ucar, Gulberk; Ulubayram, Kezban

    2015-01-01

    Targeted delivery of therapeutics is the favourable idea, whereas it is possible to distribute the therapeutically active drug molecule only to the site of action. For this purpose, in this study, catalase encapsulated poly(D,L-lactide-co-glycolide)-block-poly(ethylene glycol) (PLGA-b-PEG) nanoparticles were developed and an endothelial target molecule (anti-ICAM-1) was conjugated to this carrier system in order to decrease the oxidative stress level in the target site. According to the enzymatic activity results, initial catalase activity of nanoparticles was increased from 27.39 U/mg to up to 45.66 U/mg by adding 5 mg/mL bovine serum albumin (BSA). After 4 h, initial catalase activity was preserved up to 46.98% while free catalase retained less than 4% of its activity in proteolytic environment. Furthermore, FITC labelled anti-ICAM-1 targeted catalase encapsulated nanoparticles (anti-ICAM-1/CatNPs) were rapidly taken up by cultured endothelial cells and concomitantly endothelial cells were resistant to H2O2 induced oxidative impairment.

  3. Identification of Peptides Inhibiting Adhesion of Monocytes to the Injured Vascular Endothelial Cells through Phage-displaying Screening

    Institute of Scientific and Technical Information of China (English)

    Yu GUO; Jia ZHANG; Ji-Cheng WANG; Feng-Xiang YAN; Bing-Yang ZHU; Hong-Lin HUANG; Duan-Fang LIAO

    2005-01-01

    Using oxidized low-density lipoprotein (LDL)-injured vascular endothelial cells (ECs) as target cells, peptides specifically binding to the injured ECs were screened from a phage-displaying peptide library by using the whole-cell screening technique after three cycles of the "adsorption-elution-amplification"procedure. Positive phage clones were identified by ELISA, and the inserted amino acid sequences in the displaying peptides were deduced from confirmation with DNA sequencing. The adhesion rate of ECs to monocytes was evaluated by cell counting. The activity of endothelial nitric oxide synthase (eNOS), and the expression levels of caveolin- 1 and intercellular adhesion molecule- 1 (ICAM- 1) were determined by Western blotting. Six positive clones specifically binding to injured ECV304 endothelial cells were selected from fourteen clones. Interestingly, four phages had peptides with tandem leucine, and two of these even shared an identical sequence. Functional analysis demonstrated that the YCPRYVRRKLENELLVL peptide shared by two clones inhibited the expression of ICAM-1, increased nitric oxide concentration in the culture media, and upregulated the expression of caveolin-1 and eNOS. As a result, the adhesion rate of monocytes to ECV304 cells was significantly reduced by 12.1%. These data suggest that the anti-adhesion effect of these novel peptides is related to the regulation of the caveolin-1/nitric oxide signal transduction pathway, and could be of use in potential therapeutic agents against certain cardiovascular diseases initiated by vascular endothelial cell damage.

  4. Genome-wide association analysis of soluble ICAM-1 concentration reveals novel associations at the NFKBIK, PNPLA3, RELA, and SH2B3 loci

    NARCIS (Netherlands)

    G. Paré (Guillaume); P.M. Ridker (Paul); L.M. Rose (Lynda); M. Barbalic (maja); J. Dupuis (Josée); A. Dehghan (Abbas); J.C. Bis (Joshua); E.J. Benjamin (Emelia); D. Shiffman (Dov); A.N. Parker (Alexander); D.I. Chasman (Daniel)

    2011-01-01

    textabstractSoluble ICAM-1 (sICAM-1) is an endothelium-derived inflammatory marker that has been associated with diverse conditions such as myocardial infarction, diabetes, stroke, and malaria. Despite evidence for a heritable component to sICAM-1 levels, few genetic loci have been identified so far

  5. Research on the Relationship Between Commen Changes of Coating of Tongue and the Expression Level of ICAM-1%常见舌苔变化与ICAM-1表达水平的关系研究

    Institute of Scientific and Technical Information of China (English)

    丁兴; 詹瑧

    2007-01-01

    目的:研究常见舌苔变化与ICAM-1表达水平之间的关系.方法:应用RealtimePCR方法,对ICAM-1在正常舌苔和常见病理性舌苔中的表达进行检测.结果:ICAM-1在病理性舌苔中的表达高于在正常舌苔中的表达,其中在黄苔中的表达又高于在白苔中的表达.结论:ICAM-1表达水平的高低与舌苔厚度以及舌苔颜色的变化密切相关.

  6. The effect of lidocaine on neutrophil CD11b/CD18 and endothelial ICAM-1 expression and IL-1beta concentrations induced by hypoxia-reoxygenation.

    LENUS (Irish Health Repository)

    Lan, W

    2012-02-03

    BACKGROUND: Lidocaine has actions potentially of benefit during ischaemia-reperfusion. Neutrophils and endothelial cells have an important role in ischaemia-reperfusion injury. METHODS: Isolated human neutrophil CD11b and CD18, and human umbilical vein endothelial cell (HUVEC) ICAM-1 expression and supernatant IL-1beta concentrations in response to hypoxia-reoxygenation were studied in the presence or absence of different concentrations of lidocaine (0.005, 0.05 and 0.5 mg mL(-1)). Adhesion molecule expression was quantified by flow cytometry and IL- 1beta concentrations by ELISA. Differences were assessed with analysis of variance and Student-Newman-Keuls as appropriate. Data are presented as mean+\\/-SD. RESULTS: Exposure to hypoxia-reoxygenation increased neutrophil CD11b (94.33+\\/-40.65 vs. 34.32+\\/-6.83 mean channel fluorescence (MCF), P = 0.02), CD18 (109.84+\\/-35.44 vs. 59.05+\\/-6.71 MCF, P = 0.03) and endothelial ICAM-1 (146.62+\\/-16.78 vs. 47.29+\\/-9.85 MCF, P < 0.001) expression compared to normoxia. Neutrophil CD18 expression on exposure to hypoxia-reoxygenation was less in lidocaine (0.005 mg mL(-1)) treated cells compared to control (71.07+\\/-10.14 vs. 109.84+\\/-35.44 MCF, P = 0.03). Endothelial ICAM-1 expression on exposure to hypoxia-reoxygenation was less in lidocaine (0.005 mg mL(-1)) treated cells compared to control (133.25+\\/-16.05 vs. 146.62+\\/-16.78 MCF, P = 0.03). Hypoxia-reoxygenation increased HUVEC supernatant IL-1beta concentrations compared to normoxia (3.41+\\/-0.36 vs. 2.65+\\/-0.21 pg mL(-1), P = 0.02). Endothelial supernatant IL-1beta concentrations in lidocaine-treated HUVECs were similar to controls. CONCLUSIONS: Lidocaine at clinically relevant concentrations decreased neutrophil CD18 and endothelial ICAM-1 expression but not endothelial IL-1beta concentrations.

  7. The investigation of serum procalcitonin, hs-CRP and ICAM-1 in thediagnosis of the neonatal infection%PCT,hs-CRP与ICAM-1在新生儿感染诊断价值的探讨

    Institute of Scientific and Technical Information of China (English)

    吴达党

    2011-01-01

    目的 评价血清降钙素原(PCT),超敏C反应蛋白(hs-CRP)和淋巴细胞黏附因子-1(intercellularadhesionmolecule-1,ICAM-1)的检测在新生儿感染的临床诊断价值.方法 采用ELISA法检测PCT和ICAH-1,速率散射比浊法检测hs-CRP.结果 中、重型新生儿感染组血液中PCT,hs-CRP与ICAM-1浓度明显高于对照组和轻型感染组,差异具有统计学意义(P<0.01):ICAM-1诊断细菌感染的敏感度为81.5%,特异度为85.7%,PCT诊断细菌感染的敏感度力96.3%,特异度为92.9%,感染组ICAM-1、PCT与hs-CRP呈正相关.结论 PCT对于严重感染性疾病的诊断较ICAM-1敏感,联合PCT,hs-cRP与ICAM-1测定能够更早更灵敏地诊断新生儿感染.

  8. 缬沙坦对ox-LDL诱导的人ICAM-1表达的影响%Effect of Valsartan on ICAM-1 in Cultured HUVECs with the Ox-LDL

    Institute of Scientific and Technical Information of China (English)

    姜立清; 胡大一

    2009-01-01

    目的:检测经氧化低密度脂蛋白(ox-LDL)干预后内皮细胞细胞间粘附分子-1(ICAM-1)mRNA的表达观察缬沙坦(Valsartan)对ICAM-1 mRNA表达的影响.方法:体外培养人脐静脉内皮细胞生长到融合状态时加入ox-LDL,对照组不加任何干预,作用24小时后,分别加入不同浓度的缬沙坦继续培养24小时,测定ICAM-1 mRNA的表达.结果:Ox-LDL可诱导内皮细胞ICAM-1 mRNA的表达,不同浓度的缬沙坦可抑制ox-LDL诱导的ICAM-1 mRNA的表达(P均<0.05),并呈浓度依赖性.结论:缬沙坦抗炎及稳定动脉粥样硬化斑块的作用可能与抑制内皮细胞ICAM-1的表达有关.

  9. Expression of ICAM-1 on liver tissue from rat with acute rejection and its significance%ICAM-1在同种大鼠肝移植物中的表达及其意义

    Institute of Scientific and Technical Information of China (English)

    陈耿臻; 沈文律; 夏仁品; 文军

    2005-01-01

    目的细胞粘附现象与移植免疫排斥的关系愈来愈为人们所关注,本研究通过对细胞间粘附分子-1(ICAM-1)在大鼠同种肝移植物中的表达情况的分析,探讨ICAM-1与急性肝移植排斥反应的关系.方法采用免疫组织化学技术ABC法检测大鼠30例移植肝组织ICAM-1的表达.结果肝细胞膜、胆管上皮及炎性细胞均有大量的ICAM-1表达,中央静脉内皮细胞呈低表达,而正常大鼠肝细胞无ICAM-1表达.结论大鼠肝移植后ICAM-1在移植肝组织中的诱导表达可能是产生急性排斥的主要步骤,其机制可能是通过促进移植物浸润细胞的粘附而加剧移植排斥反应的进程.

  10. Changes of ICAM-1 and VEGF Levels in Peritoneal Fluid of Patients with Endometriosis%子宫内膜异位症患者腹腔液ICAM-1和VEGF水平的变化

    Institute of Scientific and Technical Information of China (English)

    方小玲; 夏晓梦; 林秋华

    2003-01-01

    〖目的〗通过测定子宫内膜异位症(内异症)患者腹腔液中细胞内粘附分子-1(ICAM-1)和血管内皮生长因子(VEGF)的水平,探讨其临床意义.〖方法〗采用ELISA法检测36例子宫内膜异位症患者和40例对照组腹腔液中ICAM-1和VEGF的含量.〖结果〗内异症组腹腔液中ICAM-1和VEGF的水平较对照组显著增高(均P<0.01);在月经周期中,ICAM-1的水平增殖期与分泌期差异无显著性(P>0.05),VEGF的水平增殖期显著高于分泌期(P<0.05);ICAM-1和VEGF两者无相关性(P>0.05).〖结论〗内异症患者腹腔液中ICAM-1和VEGF增高,可能参与其病变的发生发展.

  11. Study on relationship between ICAM-1 expression and biological action of bladder carcinoma%ICAM-1表达与膀胱癌生物学行为关系的研究

    Institute of Scientific and Technical Information of China (English)

    李然伟; 于颖; 李健

    1999-01-01

    目的:研究ICAM-1表达与膀胱癌生物学行为的关系.方法:应用免疫组化法对40例石蜡包埋的膀胱癌标本中ICAM-1表达进行检测.结果:膀胱癌组织中ICAM-1表达阳性率为88%,而安全缘组织中阳性率为16%,两者之间差异非常显著,且ICAM-1的表达与膀胱癌的临床分期与病理分级呈负相关,即随膀胱癌的临床分期和病理分级的增高ICAM-1表达降低.结论:膀胱癌组织ICAM-1表达检测可以作判定患者机体免疫功能状态、治疗效果及预后观察的客观指标.

  12. Expression of ICAM-1 in glioma of human brain and its clinical significance%ICAM-1在人脑胶质瘤的表达及临床意义

    Institute of Scientific and Technical Information of China (English)

    余惠平; 张和平; 田进军

    2008-01-01

    目的 探讨ICAM-1在人脑胶质瘤的表达及临床意义.方法 采用免疫组织化学法检测胶质瘤组织中ICAM-1的表达情况.结果 82例人脑胶质瘤腊块组织中全部呈ICAM-1阳性表达,阳性率100%.实验对照为脑外伤手术减压的脑组织11例,未见ICAM-1表达.胶质瘤高度恶性组ICAM-1阳性表达强度高于低度恶性组,差异有显著性(P0.05).结论 ICAM-1可能在胶质瘤的发生、发展及恶性变中发挥着一定的作用,并有助于胶质瘤恶性度分级及预后判断.

  13. Vascular Endothelial Growth Factor And Soluble Adhesion Molecules As A Diagnostic Markers For Spontaneous Bacterial Peritonitis In Cirrhotic Liver Disease

    Directory of Open Access Journals (Sweden)

    Hamdia Ezzat Ahmed, (2Ahmed Dorrah,

    2006-03-01

    Full Text Available Spontaneous bacterial peritonitis (SBP is a frequent and severe complication in cirrhotic patients with ascites that usually results in renal failure and death despite the efficacy of the current antibiotic therapy. The aim of this study was determine serum and ascitic fluid of soluble-L selectin (s-L Selectin, intracellular adhesion molecule-1 (ICAM-1, Vascular cell adhesion molecule-1 (VCAM-1 and vascular endothelial growth factor (VEGF in cirrhotic patients, and to search for a relationship between them and SBP. This study was performed on 30 cirrhotic patients with SBP. Their ages ranged (from 38-55 years with mean of (32 + 5.5, 30 cirrhotic patients with non-infected ascites; their ages ranged (from 30-52 years with mean of (35 + 6.5. This group considered as cirrhotic control group and 20 healthy control subjects their ages ranged (from 28-55 years with mean of (30 + 7.5. Serum and ascitic fluid of adhesion molecules as well as VEGF levels were significantly higher in cirrhotic patients with SBP as well as cirrhotic patients with non-infected ascites as compared to healthy control group. There were significant increase in serum and ascitic fluid level of leukocyte, PMN and ICAM-1 in SBP as compared to cirrhotic with non-infected ascites. There was non-significant decrease in serum and AF level of VEGF in cirrhotic control group as compared to SBP group. The ascitic fluid PMN and s-L Selectin were higher in culture positive SBP patients particularly in those with gram positive isolates, where these are non-significant increase in serum and ascitic fluid level of VEGF in culture positive SBP than culture negative cases. Positive correlation was found between serum and ascitic fluid level of ICAM-1 in SBP and non-infected cirrhotic group. Also, positive correlation was found between VEGF levels in serum ascetic fluid levels in both cirrhotic groups (SBP and non-infected cirrhotic group. These data suggest that: Significant elevated level of

  14. The effect of lidocaine on in vitro neutrophil and endothelial adhesion molecule expression induced by plasma obtained during tourniquet-induced ischaemia and reperfusion.

    LENUS (Irish Health Repository)

    Lan, W

    2012-02-03

    BACKGROUND: Changes in neutrophil and endothelial adhesion molecule expression occur during perioperative ischaemia and reperfusion (I\\/R) injury. We investigated the effects of lidocaine on neutrophil-independent changes in neutrophil and endothelial adhesion molecule expression associated with tourniquet-induced I\\/R. METHODS: Plasma was obtained from venous blood samples (tourniquet arm) taken before (baseline), during, 15 min, 2 and 24 h following tourniquet release in seven patients undergoing elective upper limb surgery with tourniquet application. Isolated neutrophils from healthy volunteers (n = 7) were pretreated in the presence or absence of lidocaine (0.005, 0.05 and 0.5 mg mL(-1) for 1 h, and then incubated with I\\/R plasma for 2 h. Human umbilical vein endothelial cells (HUVECs) were pretreated in the presence or absence of lidocaine (0.005, 0.05 and 0.5 mg mL(-1)) for 1 h, and then incubated with the plasma for 4 h. Adhesion molecule expression was estimated using flow cytometry. Data were analysed using ANOVA and post hoc Student-Newman-Keuls tests. RESULTS: I\\/R plasma (withdrawn 15 min following tourniquet release) increased isolated neutrophil CD11b (P = 0.03), CD18 (P = 0.01) and endothelial intercellular adhesion molecule-1 (ICAM-1) (P = 0.008) expression compared to baseline. CD11b, CD18 and ICAM-1 expression on lidocaine (0.005 mg mL(-1)) treated neutrophils was similar to control. CD11b (P < 0.001), CD18 (P = 0.03) and ICAM-1 (P = 0.002) expression on lidocaine (0.05 mg mL(-1)) treated neutrophils and HUVECs was less than that on controls. CONCLUSION: Increased in vitro neutrophil and endothelial cell adhesion molecule expression on exposure to plasma obtained during the early reperfusion phase is diminished by lidocaine at greater than clinically relevant plasma concentrations.

  15. Cilostazol decreases the expression of ICAM-1 and VCAM-1 in the retina via up-regulating PPAR-γ in diabetic rats%西洛他唑对糖尿病大鼠视网膜ICAM-1和VCAM-1的影响及其机制

    Institute of Scientific and Technical Information of China (English)

    胡建廷; 王汝霞; 高聆

    2011-01-01

    目的:观察西洛他唑对糖尿病大鼠视网膜细胞间黏附分子-1(ICAM-1)和血管细胞黏附分子-1(VCAM-1)表达的影响,并探讨其可能的作用机制.方法:以链脲佐菌素(STZ)诱发大鼠糖尿病.大鼠被随机分为正常对照组、糖尿病模型对照组、西洛他唑高剂量(27 mg·kg-1·d-1)和低剂量(9 mg·kg-1·d-1)组.西洛他唑治疗12周后测定血糖和糖化血红蛋白(HbAlc);利用RT-PCR和Western blot技术检测视网膜组织中ICAM-1,VCAM-1,过氧化物酶体增殖物激活受体γ(PPAR-γ)mRNA和蛋白质的表达.结果:与糖尿病模型对照组相比,西洛他唑能显著降低ICAM-1和VCAM-1 mRNA以及蛋白表达水平;西洛他唑治疗后,PPAR-γ mRNA和蛋白表达水平明显提高.结论:西洛他唑降低糖尿病大鼠视网膜ICAM-1和VCAM-1表达的作用可能与上调PPAR-γ有关.%Objective: To observe the effect of cilostazol on ICAM-1 and VCAM-1 expression in the retina of diabetic rats and to explore the possible mechanism. Methods: Diabetes was induced by STZ in rats. The rats were randomly divided into four groups, and treated with or without cilostazol (9 and 27 mg·kg -1 ·d -1 ). After 12week treatment, blood glucose and HbAlc were determined in all rats. The mRNA expressions of ICAM-1, VCAM1 and PPAR-γ were detected by RT-PCR; their protein expressions were detected by Western blot. Results: Compared with diabetic control, cilostazol depressed the mRNA and protein expressions of ICAM-1 and VCAM-1, but markedly enhanced the mRNA and protein expression of PPAR-γ. Conclusion: Cilostazol depresses adhesion molecule expression in the retina of diabetic rats; this is probably due to up-regulating PPAR-γ.

  16. 肝星状细胞的不同状态与ICAM-1的表达

    Institute of Scientific and Technical Information of China (English)

    陆伦根; 曾民德; 李继强; 邱德凯; 华静; 范竹萍

    1998-01-01

    目的:探讨肝星状细胞(HSC)的活化与细胞间粘附分子-1(ICAM-1)表达的关系。方法:用链酶蛋白酶和胶原酶原位灌流,Nycodenz密度梯度离心分离大鼠HSC,并进行体外培养,应用免疫组织化学方法观察静息或活化状态下的HSC中ICAM-1表达、结果:静息的HSC不表达ICAM-1,而活化的HSC表达ICAM-1,且随着培养时间的延长ICAM-1表达量逐渐增加。结论:ICAM-1表达与HSC活化及肝纤维化的发生有关。

  17. Glossogyne tenuifolia Extract Inhibits TNF-α-Induced Expression of Adhesion Molecules in Human Umbilical Vein Endothelial Cells via Blocking the NF-kB Signaling Pathway.

    Science.gov (United States)

    Hsuan, Chin-Feng; Hsu, Hsia-Fen; Tseng, Wei-Kung; Lee, Thung-Lip; Wei, Yu-Feng; Hsu, Kwan-Lih; Wu, Chau-Chung; Houng, Jer-Yiing

    2015-01-01

    Chronic inflammation plays a pivotal role in the development of atherosclerosis, where the pro-inflammatory cytokine-induced expression of endothelial adhesion molecules and the recruitment of monocytes are the crucial events leading to its pathogenesis. Glossogyne tenuifolia ethanol extract (GTE) is shown to have potent anti-inflammatory and antioxidant activities. We evaluated the effects of GTE and its major components, luteolin (lut), luteolin-7-glucoside (lut-7-g), and oleanolic acid (OA) on TNF-α-induced expression of adhesion molecules in human umbilical vein endothelial cells (HUVECs). The results demonstrated that GTE, lut, and lut-7-g attenuated the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in TNF-α-activated HUVECs, and inhibited the adhesion of monocytes to TNF-α-activated HUVECs. The TNF-α-induced mRNA expression of ICAM-1 and VCAM-1 was also suppressed, revealing their inhibitory effects at the transcriptional level. Furthermore, GTE, lut, and lut-7-g blocked the TNF-α-induced degradation of nuclear factor-kB inhibitor (IkB), an indicator of the activation of nuclear factor-kB (NF-kB). In summary, GTE and its bioactive components were effective in preventing the adhesion of monocytes to cytokine-activated endothelium by the inhibition of expression of adhesion molecules, which in turn is mediated through blocking the activation and nuclear translocation of NF-kB. The current results reveal the therapeutic potential of GTE in atherosclerosis. PMID:26393541

  18. Glossogyne tenuifolia Extract Inhibits TNF-α-Induced Expression of Adhesion Molecules in Human Umbilical Vein Endothelial Cells via Blocking the NF-kB Signaling Pathway

    Directory of Open Access Journals (Sweden)

    Chin-Feng Hsuan

    2015-09-01

    Full Text Available Chronic inflammation plays a pivotal role in the development of atherosclerosis, where the pro-inflammatory cytokine-induced expression of endothelial adhesion molecules and the recruitment of monocytes are the crucial events leading to its pathogenesis. Glossogyne tenuifolia ethanol extract (GTE is shown to have potent anti-inflammatory and antioxidant activities. We evaluated the effects of GTE and its major components, luteolin (lut, luteolin-7-glucoside (lut-7-g, and oleanolic acid (OA on TNF-α-induced expression of adhesion molecules in human umbilical vein endothelial cells (HUVECs. The results demonstrated that GTE, lut, and lut-7-g attenuated the expression of intercellular adhesion molecule-1 (ICAM-1 and vascular cell adhesion molecule-1 (VCAM-1 in TNF-α-activated HUVECs, and inhibited the adhesion of monocytes to TNF-α-activated HUVECs. The TNF-α-induced mRNA expression of ICAM-1 and VCAM-1 was also suppressed, revealing their inhibitory effects at the transcriptional level. Furthermore, GTE, lut, and lut-7-g blocked the TNF-α-induced degradation of nuclear factor-kB inhibitor (IkB, an indicator of the activation of nuclear factor-kB (NF-kB. In summary, GTE and its bioactive components were effective in preventing the adhesion of monocytes to cytokine-activated endothelium by the inhibition of expression of adhesion molecules, which in turn is mediated through blocking the activation and nuclear translocation of NF-kB. The current results reveal the therapeutic potential of GTE in atherosclerosis.

  19. Influence of rapid atrial pacing on the expression of vascular cell adhesion molecule-1 in canines%心房快速起搏对犬血管细胞黏附分子-1表达的影响

    Institute of Scientific and Technical Information of China (English)

    李佳; 葛海龙; 陈光远; 高倩萍; 孙俊峰; 李元十; 朱立群; 曹君娴; 富路

    2011-01-01

    目的 研究心房快速起搏犬模型血管细胞黏附分子-1(vascular cell adhesion molecule-1,VCAM-1)的表达.方法 选用成年健康杂种犬13条,随机分为两组:快速起搏组7条,假手术组6条.两组均开胸于右心耳缝植AOO型起搏器,快速起搏组以400 bpm起搏6周,假手术组不起搏.应用酶联免疫法测定血清VCAM-1水平,采用逆转录-多聚酶链反应(RT-PCR)测定左房组织的VCAM-1 mRNA表达水平,同时进行左房的病理分析.结果 快速起搏组犬起搏6周后的血清VCAM-1水平明显高于假手术组(t=11.63,P<0.01),左房的VCAM-1 mRNA表达水平明显高于假手术组,增高32.1%(t=2.49,P=0.03);病理结果示快速起搏组犬左房心肌细胞变性.结论 心房快速起搏可引起犬血清VCAM-1及左房VCAM-1 mRNA表达水平增高.VCAM-1可能参与心房损伤时的心肌重构过程.%Objective To invesligale the expression of vascular cell adhesion molecule - 1 (VCAM - 1) in canines who received lasling rapid alrial pacing. Methods 13 canines were randomly divided inlo Lwo groups; sham - operaled group ( n = 6 ) and alrial pacing group ( n = 7) . A pacemaker ( A00) was implanled Lo the right alrial appendage in each of the dogs. The dogs in alrial pacing group were paced at 400 bpm for 6 weeks while those in the sham - operaled group were not paced. Serum VCAM - 1 level was lesled by ELISA kit. VCAM - 1 gene expression in myocardium of left alrium were analyzed al the mRNA by reverse Iranscriplion polymerase chain reaction. The lefl alrium were also analyzed by palhology. Results Compared with the sham - operaled group, lasling alrial pacing rapidly increased the level of serum VCAM - 1 and the expression of VCAM - 1 al mRNA level in lefl alrium significanlly(P < 0. 05 ). Palhology showed that cell degeneralion existed in the lefl alrium in dogs of alrial pacing group. Conclusion Lasling alrial pacing rapidly can significantly increase the expression of serum VCAM - 1 and VCAM - 1 al m

  20. Value of knee skin temperature measured by infrared thermography and soluble intercellular adhesion molecule-1 in the diagnosis of peri-prosthetic knee infection in Chinese individuals following total knee arthroplasty

    Institute of Scientific and Technical Information of China (English)

    Mumingjiang Yishake; Zhou Xindie; He Rongxin

    2014-01-01

    Background Total knee arthroplasty (TKA) is a successful and frequently performed procedure in orthopedic surgery.The diagnosis of peri-prosthetic joint infection following TKA remains challenging.The present study estimated the usefulness of knee skin temperature (measured by infrared thermography) and serum soluble intercellular adhesion molecule-1 (slCAM-1) in the diagnosis of post-operative knee peri-prosthetic infection.Methods Patients were divided into three groups:21 patients undergoing uncomplicated TKAs,seven with prosthesis infection,and three undergoing TKA revisions.The serum levels of interleukin-6 (IL-6),C-reactive protein (CRP),erythrocyte sedimentation rate (ESR),and slCAM-1 as well as the local knee skin temperature were measured preoperatively and on Days 1 and 7 and at 1,3,and 6 months post-operatively in Groups 1 and 3.The same parameters were measured in Group 2 at the time of prosthesis infection diagnosis.Results In Group 1,the levels of IL-6,CRP,ESR,and knee skin temperature were significantly elevated post-operatively,but returned to baseline levels within 6 months.The slCAM-1 levels were not significantly different.The mean differential temperature (MDT) and levels of siCAM-1,IL-6,CRP,and ESR differed significantly between Groups 1 and 2.The MDT had returned to normal in Group 3 by 6 months post-operatively.Conclusions Elevations in IL-6,CRP,ESR,and MDT in patients undergoing TKA could be a normal response to surgical trauma,but sustained elevations may be indicative of complications.The knee skin temperature and slCAM-1 may be used as indicators in the diagnosis of knee prosthesis infection following TKA.

  1. 细胞间粘附分子-1、E-选择素及肿瘤坏死因子和慢性阻塞性肺疾病的关系%The Relationship of Intercellular Adhesion Molecules-1,E-selectin with Chronic Obstructive Pulmonary Disease

    Institute of Scientific and Technical Information of China (English)

    马希刚; 曹相原

    2006-01-01

    目的研究细胞间黏附分子(ICAM-1)、E选择素(E-selectin)和肿瘤坏死因子(TNF-α)与慢性阻塞性肺疾病(COPD)发病之间的关系.方法采用酶联免疫吸附双抗体夹心法原理(ELISA),分别检测45例COPD急性加重期患者和20例健康体检者(对照组)血清可溶性ICAM-1(sICAM-1)、可溶性E-selectin(sE-selectin)和TNF-α的含量.结果 COPD急性加重期患者血清sICAM-1和sE-selectin的平均含量明显高于对照组(P<0.001),并随着阻塞程度的加重而升高(P<0.01);TNF-α与sICAM-1和sE-selectin呈正相关(r=0.899、0.781,P<0.001).结论 ICAM-1和E-selectin参与了COPD的发生和发展,TNF-α是COPD急性加重期诱导ICAM-1和E-selectin表达上调的重要细胞因子.

  2. sICAM-1、sE-selectin水平在肝癌诊疗中的价值①%The value of measurement of sICAM-1 and sE-selectin in hepatocellular carcinom a (HCC)

    Institute of Scientific and Technical Information of China (English)

    唐南洪; 陈燕凌; 李秀金; 王晓茜; 殷凤峙

    2001-01-01

    目的:探讨血清细胞间粘附分子-1(sICAM-1)、E-选择素(sE-selectin)在肝癌诊疗中的价值.方法:检测健康人、慢胜肝炎、肝硬化、肝癌者手术前后sICAM-1、sE-selectin水平变化.结果:79例各期肝癌者总体sICAM-1、SE-selectin水平明显高于慢性肝炎、肝硬化和健康对照组(P<0.01),但Ⅰ期肝癌组与慢性肝炎、肝硬化组比较无显著差异;各期肝癌术后sICAM1-1及Ⅰ、Ⅱ、Ⅲ期肝癌术后sE-selectin水平均较术前明显下降.结论:提示早期肝癌患者检测血清sICAM-1、sE-selectin无确诊意义 ,但可作为中、晚期肝癌者特别是AFP阴性患者的血清学确诊参考和预后的监测指标.

  3. 大肠癌PARP表达与P-selectin和ICAM-1表达的相关性%Correlation of PARP expression with P-selectin and ICAM-1 expression in colorectal carcinoma

    Institute of Scientific and Technical Information of China (English)

    郝兰香; 王娅兰; 李圆圆

    2006-01-01

    目的 初步探讨聚腺苷二磷酸核糖聚合酶(PARP)与大肠癌侵袭转移的关系及其可能机制.方法 采用SP免疫组化法检测PAR(聚腺苷二磷酸核糖,系PARP产物)、P-selectin及ICAM-1的表达;并应用免疫荧光双标法检测PAR与P-selectin、ICAM-1的共表达.结果 大肠癌组织内PAR、P-selectin及ICAM-1的表达均明显高于对照肠黏膜(P<0.05);3种蛋白的表达仅与大肠癌转移有关(P<0.05),而与其他临床病理因素无关;PAR与P-selectin和ICAM-1的表达均呈正相关关系(P<0.05).结论 大肠癌组织内PARP活性增强,并可能通过上调P-selectin和ICAM-1的表达而有利于大肠癌侵袭转移,有望成为判断大肠癌转移的参考指标之一.

  4. White blood cell deformation and firm adhesion

    Science.gov (United States)

    Szatmary, Alex; Eggleton, Charles

    2011-11-01

    For a white blood cell (WBC) to arrive at infection sites, it forms chemical attachments with activated endothelial cells. First, it bonds with P-selectin, which holds it to the wall, but weakly; this allows the WBC to roll under the shear flow of the blood around it. Later, the WBCs bond with the stronger intracellular adhesion molecule-1 (ICAM-1); it is these ICAM bonds that allow the WBCs to fully resist the flow and stop rolling, allowing them to crawl through the endothelial wall. We model this numerically. Our model uses the immersed boundary method to represent the interaction of the shear flow with the deformable cell membrane. Receptors are on the tips of microvilli-little fingers sticking off of the cell membrane. The microvilli also deform. The receptors stochastically form and break bonds with molecules on the wall. Using this method, the history of each microvillus and its bonds can be found, as well as the distribution of the adhesion traction forces and how all of these vary with the deformability of the white blood cell. At higher shear rates, the white blood cell membrane deforms more, increasing its contact area with the surface; this effect is larger for softer membranes. We investigate how the deformability of the WBC affects the ease with which it forms firm adhesion.

  5. Family with sequence similarity 5, member C (FAM5C increases leukocyte adhesion molecules in vascular endothelial cells: implication in vascular inflammation.

    Directory of Open Access Journals (Sweden)

    Junya Sato

    Full Text Available Identification of the regulators of vascular inflammation is important if we are to understand the molecular mechanisms leading to atherosclerosis and consequent ischemic heart disease, including acute myocardial infarction. Gene polymorphisms in family with sequence similarity 5, member C (FAM5C are associated with an increased risk of acute myocardial infarction, but little is known about the function of this gene product in blood vessels. Here, we report that the regulation of the expression and function of FAM5C in endothelial cells. We show here that FAM5C is expressed in endothelial cells in vitro and in vivo. Immunofluorescence microscopy showed localization of FAM5C in the Golgi in cultured human endothelial cells. Immunohistochemistry on serial sections of human coronary artery showed that FAM5C-positive endothelium expressed intercellular adhesion molecule-1 (ICAM-1 or vascular cell adhesion molecule-1 (VCAM-1. In cultured human endothelial cells, the overexpression of FAM5C increased the reactive oxygen species (ROS production, nuclear factor-κB (NF-κB activity and the expression of ICAM-1, VCAM-1 and E-selectin mRNAs, resulting in enhanced monocyte adhesion. FAM5C was upregulated in response to inflammatory stimuli, such as TNF-α, in an NF-κB- and JNK-dependent manner. Knockdown of FAM5C by small interfering RNA inhibited the increase in the TNF-α-induced production of ROS, NF-κB activity and expression of these leukocyte adhesion molecule mRNAs, resulting in reduced monocyte adhesion. These results suggest that in endothelial cells, when FAM5C is upregulated in response to inflammatory stimuli, it increases the expression of leukocyte adhesion molecules by increasing ROS production and NF-κB activity.

  6. Sequential expression of adhesion and costimulatory molecules in graft-versus-host disease target organs after murine bone marrow transplantation across minor histocompatibility antigen barriers.

    Science.gov (United States)

    Eyrich, Matthias; Burger, Gudrun; Marquardt, Katja; Budach, Wilfried; Schilbach, Karin; Niethammer, Dietrich; Schlegel, Paul G

    2005-05-01

    Graft-versus-host disease (GVHD) is a potentially fatal complication after allogeneic bone marrow transplantation. However, few data exist thus far on the molecular signals governing leukocyte trafficking during the disease. We therefore investigated the sequential pattern of distinct adhesion, costimulatory, and apoptosis-related molecules in GVHD organs (ileum, colon, skin, and liver) after transplantation across minor histocompatibility barriers (B10.D2 --> BALB/c, both H-2d). To distinguish changes induced by the conditioning regimen from effects achieved by allogeneic cell transfer, syngeneic transplant recipients (BALB/c --> BALB/c) and irradiated nontransplanted mice were added as controls. Irradiation upregulated the expression of vascular cell adhesion molecule (VCAM)-1, intercellular adhesion molecule (ICAM)-l, and B7-2 in ileum, as well as VCAM-1 and B7-2 in colon, on day 3 in all animals. Whereas in syngeneic mice these effects were reversed from day 9 on, allogeneic recipients showed further upregulation of VCAM-1, ICAM-1, B7-1, and B7-2 in these organs on day 22, when GVHD became clinically evident. Infiltration of CD4+ and CD8+ donor T cells was noted on day 9 in skin and liver and on day 22 in ileum and colon. Surprisingly, the expression of several other adhesion molecules, such as ICAM-2, platelet-endothelial cell adhesion molecule 1, E-selectin, and mucosal addressin cell adhesion molecule 1, did not change. Proapoptotic and antiapoptotic markers were balanced in GVHD organs with the exception of spleen, in which a preferential expression of the proapoptotic Bax could be noted. Our results indicate that irradiation-induced upregulation of VCAM-1, ICAM-1, and B7-2 provides early costimulatory signals to incoming donor T cells in the intestine, followed by a cascade of proinflammatory signals in other organs once the alloresponse is established.

  7. 阿司匹林对胃肠黏膜损伤ICAM-1表达的临床研究%Clinical research on aspirin for damage in bronchia mucosal the ICAM-1 express

    Institute of Scientific and Technical Information of China (English)

    严孚莹

    2010-01-01

    目的:探讨阿司匹林对胃肠黏膜损伤ICAM-1表达的临床意义.方法:应用免疫组化检测ICAM-1在大鼠胃黏膜细胞的表达.结果:实验组应用5.021mg/kg阿司匹林灌胃3d后,开始出现胃黏膜损伤的表现,损伤指数为(9.07±0.64)mm,14d损伤达高峰,损伤指数为(23.49±0.57)mm.免疫组化结果显示ICAM-1在用药后3d开始表达,7d后逐渐升高,21d达高峰,28d及35d仅有少量表达.实验组用药后与用药前比较ICAM-1表达水平有明显差异;对照组与实验组比较,ICAM-1均明显呈低水平表达.结论:在阿司匹林引起的胃黏膜损伤过程中ICAM-1的表达有一定的临床意义.阿司匹林对胃黏膜有较为明显的损伤,具有一定的危险性.

  8. 槲皮素对人血管内皮细胞中ICAM-1表达的影响%Quercetin Inhibits IL-1 β Induced ICAM-1 Expression in Human Endothelial Cells

    Institute of Scientific and Technical Information of China (English)

    唐永江

    2007-01-01

    目的: 研究槲皮素对血管炎症中的细胞间黏附因子-1的表达影响.方法: 利用IL-1β构建细胞炎症模型,利用RT-PCR技术检测ICAM-1的mRNA水平的表达变化.结果: 槲皮素对ICAM-1具有下调作用,且具有一定的时间和浓度依赖性.

  9. 急性髓性白血病患者骨髓基质细胞ICAM-1的检测及临床意义

    Institute of Scientific and Technical Information of China (English)

    张宇明; 江黎明; 陈永振

    2004-01-01

    目的研究急性髓性白血病患者骨髓基质细胞ICAM-1水平的变化及临床意义.方法采用免疫组化法,对20例急性髓性白血病(AML)患者及正常对照组骨髓基质细胞ICAM-1水平进行检测.结果该患者骨髓基质细胞ICAM-1水平高于正常对照组.ICAM-1高组与ICAM-1低组比较,前者疗效较差.结论 ICAM-1水平的检测有助于判断患者的疗效.

  10. [Dexmedetomidine suppresses the expressions of TLR4, NF-κB and ICAM-1 mRNA in the lung of rabbits during one lung ventilation].

    Science.gov (United States)

    Bian, Qingming; Gu, Lianbing; Xu, Zeping; Li, Pengyi; Qian, Yanning; Zhu, Dongya

    2016-09-01

    Objective To investigate the effect of dexmedetomidine on lung injury and the expressions of Toll-like receptor 4 (TLR4), nuclear factor κB p65 (NF-κB p65) and intercellular adhesion molecular 1 (ICAM-1) mRNA during one-lung ventilation (OLV) in rabbits. Methods Thirty healthy New Zealand white rabbits were randomly divided into three groups ( n=10 in each group): two-lung ventilation (TLV) group (group T), OLV group (group O), dexmedetomidine used during OLV group (group D-O). The rabbits in group T were treated with TLV for 3.5 hours, while in group O and group D-O, the rabbits were ventilated through right lung for 3 hours following 30-minute TLV. In group D-O, dexmedetomidine (1 μg/kg) were given intravenously for 10 minutes before tracheostomy, followed by intravenous infusion at the rate of 1 μg/(kg.h). Equal volume of normal saline was given in group O and group T as controls. At the end of the experiment, rabbits were sacrificed and lung tissues were collected. The pulmonary wet/dry mass (W/D) ratio was calculated and the pathological changes of the lungs were observed using HE staining under a light microscope. The expressions of TLR4, NF-κB p65, ICAM-1 mRNA were analyzed by real-time quantitative PCR. Results W/D ratio of left lung tissues in group O and group D-O were significantly higher as compared with group T. However, W/D ratio in group D-O was obviously lower than that in group O. Compared with group T, both group O and group D-O showed much more serious morphological damage in the lung, and such lung injury was less obvious in group D-O than in group O. The expressions of TLR4, NF-κB p65, ICAM-1 mRNA increased significantly in group O as compared with group T, and such enhancement was ameliorated by dexmedetomidine as observed in group D-O. Conclusion Dexmedetomidine might inhibit inflammatory responses and attenuate OLV-induced lung injury in rabbits, possibly by suppressing the expressions of TLR4 and NF-κB p65 mRNA. PMID:27609575

  11. A Chinese Herbal Preparation Containing Radix Salviae Miltiorrhizae, Radix Notoginseng and Borneolum Syntheticum Reduces Circulating Adhesion Molecules

    Directory of Open Access Journals (Sweden)

    Kylie A. O’Brien

    2011-01-01

    Full Text Available Circulating adhesion molecules (CAMs, surface proteins expressed in the vascular endothelium, have emerged as risk factors for cardiovascular disease (CVD. CAMs are involved in intercellular communication that are believed to play a role in atherosclerosis. A Chinese medicine, the “Dantonic Pill” (DP (also known as the “Cardiotonic Pill”, containing three Chinese herbal material medica, Radix Salviae Miltiorrhizae, Radix Notoginseng and Borneolum Syntheticum, has been used in China for the prevention and management of CVD. Previous laboratory and animal studies have suggested that this preparation reduces both atherogenesis and adhesion molecule expression. A parallel double blind randomized placebo-controlled study was conducted to assess the effects of the DP on three species of CAM (intercellular cell adhesion molecule-1 (ICAM-1, vascular cell adhesion molecule-1 and endothelial cell selectin (E-selectin in participants with mild-moderate hypercholesterolemia. Secondary endpoints included biochemical and hematological variables and clinical effects. Forty participants were randomized to either treatment or control for 12 weeks. Treatment with DP was associated with a statistically significant decrease in ICAM-1 (9% decrease, P = .03 and E-Selectin (15% decrease, P = .004. There was no significant change in renal function tests, liver function tests, glucose, lipids or C-reactive protein levels and clinical adverse effects did not differ between the active and the control groups. There were no relevant changes in participants receiving placebo. These results suggest that this herbal medicine may contribute to the development of a novel approach to cardiovascular risk reduction.

  12. Selected immunological changes in patients with Goeckerman's therapy TNF-alpha, sE-selectin, sP-selectin, sICAM-1 and IL-8

    Energy Technology Data Exchange (ETDEWEB)

    Borska, L.; Fiala, Z.; Krejsek, J.; Andrys, C.; Vokurkova, D.; Hamakova, K.; Kremlacek, J.; Ettler, K. [Charles University, Hradec Kralove (Czech Republic). Faculty of Medicine

    2006-07-01

    Psoriasis is one of the most frequent inflammatory skin diseases in which abnormal individual immune reactivity plays an important role. The aim of the present study was to describe selected immunological changes, concerning pro-inflammatory cytokines (TNF-alpha, IL-8) and adhesion molecules (sE-selectin, sP-selectin, sICAM-1), in 56 patients cured by Goeckerman's therapy (GT). GT includes dermal application of crude coal tar (containing polycyclic aromatic hydrocarbons) and exposure to UV radiation.

  13. Monocyte chemotactic protein-1 and soluble adhesion molecules as possible prognostic markers of the efficacy of antiviral treatment in chronic hepatitis C

    Institute of Scientific and Technical Information of China (English)

    Anatol Panasiuk; Danuta Prokopowicz; Bozena Panasiuk

    2004-01-01

    AIM: To explain the role of Monocyte chemotactic protein-1 (MCP-1) and soluble adhesion molecules in chronic hepatitis C during the treatment of interferon alpha (IFNα) 2 b and ribavirin (RBV).METHODS: Concentrations of MCP-1, soluble adhesion molecules intercellular adhesion molecule-1 (sICAM-1), sPselectin, interleukin (IL) 6, and IL10 in serum were estimated in the group of 40 patients with chronic hepatitis C treated with IFNalpha2 b and RBV in 0, 16, 32, 48 wk of the therapy.RESULTS: In chronic hepatitis C, before and during the treatment, the serum levels of MCP-1 and sP-selectin in responders were similar to those of healthy subjects. In nonresponders (NR), MCP-1 increased in the course of IFNα+RBV treatment, differences were statistically significant as compared to responders. MCP-1 correlated statistically with the activity of pedportal inflammation (r = 0.35, P<0.05) but not with staging of liver fibrosis. sICAM-1 positively correlated with inflammatory activity and fibrosis in NR. sP-selectin did not correlate with histological findings in the liver. The MCP-1 correlated with the soluble form of sP-selectin concentrations (r = 6, P<0.001) and with IL-10 level in NR (r = 0.4, P<0.05). There was no correlation observed between the concentration of MCP-1 and sICAM-1, IL-6 during the treatment.CONCLUSION: MCP-1 concentration may be a prognostic marker of the efficacy of IFN+RBV therapy in patients with chronic hepatitis C.

  14. HT-29肠癌细胞中E-selectin、Integrin β1及ICAM-1表达水平%Expression of E-Selectin, Integrin β1 and ICAM-1 in HT-29 Colon Carcinoma Cells

    Institute of Scientific and Technical Information of China (English)

    刘长宝; 凌志强

    2007-01-01

    目的:探讨HT-29肠癌细胞、正常肠上皮细胞及ECV-304血管内皮细胞中E-selectin、Integrin β1及ICAM-1的表达状态.方法:采用Nothern Blotting方法检测HT-29肠癌细胞、正常肠上皮细胞和ECV-304血管内皮细胞中E-selectin、Integrin β1及ICAM-1 mRNA表达水平,采用ELISA法定量分析其表达含量.结果:HT-29肠癌细胞、正常肠上皮细胞和ECV-304血管内皮细胞均有E-selectin、Integrin β1及ICAM-1基因表达.ELISA定量测定3个粘附分子表达水平,HT-29肠癌细胞均高于正常肠上皮细胞和ECV-304血管内皮细胞,分别存在显著性差异(P<0.05).结论:E-selectin、Integrin β1、ICAM-1可能与肿瘤细胞转移有关.

  15. E-selectin和sICAM-1在儿童肺炎支原体感染中的价值%Clinical value of E-selectin and sICAM-1 in diagnosis of children with Mycoplasma Pneumoniae infection

    Institute of Scientific and Technical Information of China (English)

    李苏亮; 叶芸

    2015-01-01

    目的 探讨E-选择素( E-selectin)与可溶性细胞间黏附分子-1 ( sICAM-1 )在儿童肺炎支原体感染中的应用价值.方法 选取本院儿科急性期肺炎支原体感染的患儿48例,恢复期患儿42例,选取同期体检的40例健康儿童做为对照组,采用ELISA法测定血浆E-selectin和sICAM-1水平. 用ROC曲线评价E-selectin和sICAM-1对急性期肺炎支原体感染的诊断效能;将急性期患儿血浆E-selectin与sICAM-1浓度进行相关性分析. 结果 急性期患儿血浆E-selectin和sICAM-1的水平明显高于恢复期及健康对照组,差异有统计学意义(P<0. 05);E-selectin诊断急性期肺炎支原体肺炎的AUC为0. 852(95%可信区间为0. 751-0. 952),其敏感度为80. 0%,特异度为78. 5%;sICAM-1 诊断急性期肺炎支原体肺炎的 AUC为0. 859 (95%可信区间为0. 764-0. 954),其敏感度为80. 5%,特异度为80. 0%. 急性期患儿E-selectin和sICAM-1水平呈明显正相关(r=0. 758,P<0. 01). 结论 急性期肺炎支原体感染患者血浆E-selectin和sICAM-1水平显著增高,可作为评价肺炎支原体感染病情程度以及治疗疗效观察的重要指标.%Objective To explore the diagnostic value of the E-selectin and sICAM-1 in children suffering from Mycoplasma pneumoniae infection. Methods Clinical data of 48 patients with acute Mycoplasma pneumoniae infection and 42 patients in recovery phase were reviewed, and 40 healthy children were chosen as control group. ELISA was used to detect the levels of E-selectin and sICAM-1, and the receiver operating characteristic(ROC) curve was used to evaluate the diagnosis efficiency of acute Mycoplasma pneumoniae infec-tion. The correlation between E-selectin and sICAM-1 was analyzed in patients with acute Mycoplasma pneumoniae infection. Results The levels of E-selectin and sICAM-1 were significantly higher in acute Mycoplasma pneumoniae infection than those in recovery phase(P<0. 05). The area under ROC curve of E-selectin was 0. 852(95%CI 0

  16. Adenovirus viral interleukin-10 inhibits adhesion molecule expressions induced by hypoxia/reoxygenation in cerebrovascular endothelial cells1

    Institute of Scientific and Technical Information of China (English)

    Hui KANG; Peng-yuan YANG; Yao-cheng RUI

    2008-01-01

    Aim: To investigate the effects of recombinant adenovirus encoding viral interleukin-10 (vIL-10), a potent anti-inflammatory cytokine, on adhesion mol-ecule expressions and the adhesion rates of leukocytes to endothelial cells in cerebrovascular endothelial cells injured by hypoxia/reoxygenation (H/R). Methods: A recombinant adenovirus expressing vIL-10 (Ad/vIL-10 (or the green fluorescent protein (Ad/GFP) gene was constructed. A cerebrovascular endothe-lial cell line bend.3 was pretreated with a different multiplicity of infection (MOI) of Ad/vIL-10 or Ad/GFP and then exposed to hypoxia for 9 h followed by reoxygenation for 12 h. The culture supernatants were tested for the expression of vIL-10 and endogenous murine IL-10 (mIL-10) by ELISA. The effects of Ad/vIL-10 on monocyte-endothelial cell adhesion were represented as the adhesion rate. Subsequently, the expressions of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1(VCAM-1) in the endothelial cells after treat-ment with Ad/vIL-10 and H/R were analyzed by Western blotting and real-time PCR. Results: vIL-10 was expressed in cultured bEnd.3 after Ad/vIL-10 transfec-tion and was significantly increased by H/R. Ad/vIL-10 or Ad/GFP did not affect the mlL-10 level. H/R increased the mIL-10 expression, but insignificantly. Mono-cyte-endothelial cell adhesion induced by H/R was significantly inhibited by pretreatment with Ad/vIL-10 (MOI: 80). ICAM-I, and VCAM-1 in bEnd.3 and were significantly increased after H/R, while pretreatment with Ad/vIL-10 (MOI: 80) significantly inhibited their expressions. Ad/GFP did not markedly affect mono-cyte-endothelial adhesion and the expressions of ICAM-1 and VCAM-1 induced by H/R. Conclusion: Ad/vIL-10 significantly inhibits the upregulation of endot-helial adhesion molecule expressions and the increase of adhesion of monocytes-endothelial cells induced by H/R, indicating that vIL-10 gene transfer is of far-reaching significance in the therapy of

  17. 双歧杆菌LTA上调ICAM-1表达及其在LAK抗肿瘤中的作用%Upregulation of ICAM-1 expression enhances cytotoxic sensitivity of tumor cells to LAK by LTA from bifidobacterium

    Institute of Scientific and Technical Information of China (English)

    蒋虹; 胡宏; 魏启欧

    2000-01-01

    目的 探讨双歧杆菌脂磷壁酸(lipoteichoic acid,LTA)作用于LoVo细胞后是否能增强LAK对该细胞的识别 阳杀伤,以及ICAM-1在其中的作用。方法 采用MTT方法观察了LAK对LoVo细胞的识别和杀伤作用,并用流式细胞仪和 ELISA的方法检测了LoVo细胞表面ICAM-1的表达。结果 50 μg/ml LTA作用3 d,LAK对LoVo细胞的粘附率由9.62%增 加到24.42%,LoVo细胞对LAK的杀伤敏感性增加了2倍。并且使表达ICAM-1的细胞数由2.42%增加到27.9%,LoVo细胞 上ICAM-1的表达量增加10倍。结论 LTA增强了LoVo细胞对LAK的杀伤敏感性,其机制可能在于LTA通过上调LoVo细 胞上ICAM-1的表达,增强了效靶细胞之间的识别和结合。LTA与LAK相结合可能增强对大肠癌的治疗效果。%Objective To investigate whether the recognizing and cytotoxic abilities of LAK can be intensified by bifi- dobacterial lipoteichoic acid(LTA) and the possible role of ICAM-1 in this process. Methods Standard MTT assay was used to evaluate the binding rate and cytotoxic capability of LAK to LoVo cells. Flow cytometric assay and ELISA were used to deter- mine the expression of ICAM-1 on these cells. Results LAK cells bound much easier to LoVo cells with an increase from 9. 62% to 24.42% as well as a double increase of the anti-tumor sensitivity of LoVo cells to LAK after challenge with 50 μg/ml LTA of Bifidobacterium bffidum 1101. Compared with the control group,both the percentage of ICAM-1 positive cells and the amount of ICAM-1 expression on LoVo cells were greatly increased directly after the challenge of LTA. Conclusion The pos- sible mechanism of the increase of antitumor activity lies in that Bifidobacterial LTA can intensify the binding and recognizing capability of LAK to tumor cells by promoting the expression of ICAM-1 on the surface of LoVo cells. The therapeutic effect on intestinal cancer may be enhanced by the combined treatment of bifidobacterial LTA and LAK.

  18. Thymic and lymph node mesenchymal subsets can be derived from PDGFRα/β+Gp38+CD34+ICAM1- vascular adventitial precursors

    DEFF Research Database (Denmark)

    Sitnik, Katarzyna Maria; Wendland, Kerstin; Weishaupt, Holger;

    developed from a common PDGFRα/β+Gp38+CD34-ICAM1- embryonic precursor population. Notably, precursor-progeny studies involving transfer of adult thymus- and adipose tissue-derived BP3-Gp38+PDGFRα+CD34+ICAM1- cells into thymic and LN re-aggregate organ grafts uncovered a precursor activity towards not only...

  19. 大肠癌术后复发患者血清ICAM-1水平变化的临床意义

    Institute of Scientific and Technical Information of China (English)

    袁文清; 周学斌

    2012-01-01

    目的 观察大肠癌术后复发患者血清ICAM-1水平的变化,探讨其临床意义.方法 用ELISA法测定19例大肠癌术后复发患者和25例大肠癌根术后健康患者血清ICAM-1水平.结果 大肠癌术后复发患者血清ICAM-1水平明显高于正常对照组.结论 血清ICAM-1水平与大肠癌术后复发有关,临床中ICAM-1水平可作为预测大肠癌复发与否的有效指标之一.

  20. Adhesion

    Science.gov (United States)

    As the body moves, tissues or organs inside are normally able to shift around each other. This is because these tissues have ... occur if the adhesions cause an organ or body part to: Twist Pull ... unable to move normally The risk of forming adhesions is high ...

  1. 胃癌患者血清可溶性P-选择素和细胞间黏附分子-1的表达%Expression of serum soluble P-selectin and intercellar adhesion molecule-1 in patients with gastric carcinoma

    Institute of Scientific and Technical Information of China (English)

    王程虎; 张健

    2006-01-01

    目的:探讨胃癌患者手术前后血清可溶性P-选择素(sP-selectin)、细胞间黏附分子-1(sICAM-1)的表达及临床意义.方法:采用ELISA法检测40例胃癌患者术前、术后15 d、术后30 d及20例对照的血清sP-selectin、sICAM-1水平.结果:胃癌患者血清sP-selectin、sICAM-1水平均高于对照组(P<0.01);术后15 d下降,仍高于对照组水平(P<0.05);术后30 d降至对照组水平(P>0.05).血清sP-selectin、sICAM-1水平与胃癌的淋巴结转移和临床分期相关(P<0.05),与患者年龄、性别、肿瘤大小及组织学分级无明显相关(P>0.05).结论:sP-selectin、sICAM-1参与了胃癌的发生发展,可成为判断预后的一个重要指标.

  2. 大肠癌患者血清可溶性E-选择素和细胞间黏附分子-1检测%Detection of serum soluble E-selectin and intercellar adhesion molecule-1 in patients with colorectal carcinoma

    Institute of Scientific and Technical Information of China (English)

    张健; 王程虎

    2007-01-01

    目的:探讨大肠癌患者血清可溶性E-选择素(sE-selectin)、细胞间黏附分子-1(sICAM-1)检测的意义.方法:采用ELISA检测40例大肠癌患者术前、术后15 d、术后30 d及20例对照(健康体检者)血清sE-selectin、sICAM-1水平.结果:大肠癌患者术前血清sE-selectin、sICAM-1水平高于对照组(P<0.05);术后15 d下降,但仍高于对照组(P<0.05);术后30 d降至对照组水平(P>0.05).大肠癌患者血清sE-selectin、sICAM-1水平与淋巴结转移和临床分期有关(P<0.05),与年龄、性别、肿瘤大小及组织学分级无关(P>0.05).结论:sE-selectin、sICAM-1可能参与了大肠癌侵袭转移过程,是反映大肠癌发生、发展及预后的重要指标.

  3. Immunologic changes in TNF-alpha, sE-selectin, sP-selectin, sICAM-1, and IL-8 in pediatric patients treated for psoriasis with the Goeckerman regimen

    Energy Technology Data Exchange (ETDEWEB)

    Borska, L.; Fiala, Z.; Krejsek, J.; Andrys, C.; Vokurkova, D.; Hamakova, K.; Kremlacek, J.; Ettler, K. [Charles University of Prague, Hradec Kralove (Czech Republic). Faculty of Medicine

    2007-11-15

    Psoriasis is a chronic inflammatory skin disease which is often manifested during childhood. The present study investigated changes in the serum levels of proinflammatory cytokines and soluble forms of adhesion molecules in children with psoriasis. The observed patient group of 26 children was treated with the Goeckerman regimen. This therapy combines dermal application of crude coal tar with ultraviolet radiation. The Psoriasis Area Severity Index decreased significantly after treatment by with the Goeckerman regimen (p < 0.001). Serum levels of the proinflammatory cytokine TNF-alpha and adhesion molecules sICAM-1, sP-selectin and sE-selectin decreased after the Goeckerman regimen. The TNF-alpha and sICAM-1 decreased significantly (p < 0.05). Our findings support the complex role of these immune parameters in the immunopathogenesis of psoriasis in children. The serum level of IL-8 increased after the Goeckerman regimen. This fact indicates that the chemokine pathway of IL-8 activity could be modulated by this treatment, most likely by polycyclic aromatic hydrocarbons.

  4. 细胞间粘附分子-1反义DNA体外对内皮细胞细胞间粘附分子-1表达的抑制作用%Inhibitory effect of ICAM-1 antisense DNA on ICAM-1 expression in endothelial cells in vitro

    Institute of Scientific and Technical Information of China (English)

    徐洪实; 梅长林; 王琪; 陈蕾

    1999-01-01

    目的:研究细胞间粘附分子-1(ICAM-1)反义DNA对内皮细胞ICAM-1表达的抑制作用.方法:构建ICAM-1反义DNA载体,用脂质体转染内皮细胞,TNFα刺激后,流式细胞术检测转染细胞表面ICAM-1蛋白的表达.结果:酶切鉴定证明,1.4kb的ICAM-1DNA片段反向连接到pcDNA3表达载体;流式细胞术检测显示,正常细胞加TNFα刺激后,表面ICAM-1表达明显升高(P0.05),转染细胞表面ICAM-1表达低于正常细胞(P<0.05).结论:ICAM-1反义DNA体外可抑制细胞ICAM-1表达.

  5. Changes of soluble intercellular adhesion molecules-1 in children with juvenile rheumatoid arthritis%幼年型类风湿性关节炎患儿血清可溶性细胞间黏附分子-1变化

    Institute of Scientific and Technical Information of China (English)

    钱小青; 张冬玲; 赵乃琤; 曹黎明; 王大为

    2003-01-01

    目的研究可溶性细胞间黏附分子-1(sICAM-1)在幼年型类风湿性关节炎(JRA)患儿中的变化.方法用双抗体夹心ELISA方法检测38例(20 例全身型,8例多关节型和10例少关节型)活动期与缓解期JRA患儿和15例正常对照患儿血清sICAM-1水平.结果 1.活动期全身型、多关节型及少关节型JRA患儿血清sICAM-1水平均较正常对照明显增高(P<0.001),全身型较少关节炎型明显增高(P<0.05);2.治疗后全身型血清sICAM-1水平明显降低(P<0.001),但仍高于正常对照组,多关节型与少关节型治疗后sICAM-1水平较治疗前虽有下降,但无显著差异(P>0.05).结论 ICAM-1在JRA的发病机制中起一定作用,血清sICAM浓度与病变类型有关,但不适合作为病情缓解指标.

  6. Role of adhesion molecules and dendritic cells in rat hepatic/renal ischemia-reperfusion injury and anti-adhesive intervention with anti-P-selectin lectin-EGF domain monoclonal antibody

    Institute of Scientific and Technical Information of China (English)

    Tong Zhou; Gui-Zhi Sun; Ming-Jun Zhang; Jin-Lian Chen; Dong-Qing Zhang; Qing-Shen Hu; Yu-Ying Chen; Nan Chen

    2005-01-01

    AIM: To investigate the role of P-selectin, intercellular adhesion molecule-1 (ICAM-1) and dendritic cells (DCs)in liver/kidney of rats with hepatic/renal ischemiareperfusion injury and the preventive effect of anti-Pselectin lectin-EGF domain monoclonal antibody (anti-PsLEGFmAb) on the injury.METHODS: Rat models of hepatic and renal ischemiareperfusion were established. The rats were then divided into two groups, one group treated with anti-PsL-EGFmAb(n = 20) and control treated with saline (n = 20). Both groups were subdivided into four groups according to reperfusion time (1, 3, 6 and 24 h). The sham-operated group (n = 5) served as a control group. DCs were observed by the microscopic image method, while P-selectin and ICAM-1 were analyzed by immunohistochemistry.RESULTS: P-selectin increased significantly in hepatic sinusoidal endothelial cells and renal tubular epithelial cells 1 h after ischemia-reperfusion, and the expression of ICAM-1 was up-regulated in hepatic sinusoid and renal vessels after 6 h. CD1a+CD80+DCs gradually increased in hepatic sinusoidal endothelium and renal tubules and interstitium 1 h after ischemia-reperfusion, and there was the most number of DCs in 24-h group. The localization of DCs was associated with rat hepatic/renal function.These changes became less significant in rats treated with anti-PsL-EGFmAb.CONCLUSION: DCs play an important role in immune pathogenesis of hepatic/renal ischemia-reperfusion injury.Anti-PsL-EGFmAb may regulate and inhibit local DC immigration and accumulation in liver/kidney.

  7. The effects of caveolin - 1/eNOS pathway in monocyte adhesion to endothelial cells induced by oxidative stress

    Institute of Scientific and Technical Information of China (English)

    LiaoDuan-fang

    2005-01-01

    Leukocyte adhesion to endothelial cells is the initiate event of atherosclerosis, which includes injury of endothelial cells, leukocyte rolling, adhesion and extravasation. Many adhesion molecules such as E-selectin, P-selectin,the adhesion process.ICAM-1, VCAM, L-selectin, CD18, PECAM, VLA and ECM participate in Many factors such as infection of pathogenic organism,

  8. 血管性假血友病因子和细胞间黏附分子-1在急性呼吸窘迫综合征中的动态变化及早期诊断的意义%Variations and early prediction of von willebrand factor and soluble intercellular adhesion molecule-1 in acute respiratory distress syndrome

    Institute of Scientific and Technical Information of China (English)

    李锐; 曹书华; 王今达

    2004-01-01

    目的检测血管性假血友病因子、可溶性细胞间黏附分子-1浓度变化,以研究其在ARDS早期诊断中的意义.方法以ELISA法检测非ARDS组和ARDS组于0、2、3、5和7d血浆vWF和sICAM-1浓度.结果ARDS组vWF和sICAM-1浓度高于非ARDS组,前四个时点的中性粒细胞活化计数ARDS组高于非ARDS组.血浆vWF和sICAM-1水平具有相关性.结论血浆vWF和sICAM-1浓度及中性粒细胞活化计数在ARDS的早期即升高,对ARDS早期诊断有预警作用.

  9. Prevention of reovirus type 2-induced diabetes-like syndrome in DBA/1 suckling mice by treatment with antibodies against intercellular adhesion molecule-1 and lymphocyte function-associated antigen-1.

    OpenAIRE

    Hayashi, T.; Yamamoto, S.; Onodera, T.

    1995-01-01

    Reovirus type 2-induced diabetes-like syndrome in suckling mice is considered to be an animal model for human insulin-dependent diabetes mellitus. We have previously demonstrated that immunopathologic pancreatic islet cell damage might be relevant to reovirus type 2 infection. In this study the involvement of adhesion molecules in the development of reovirus type 2-induced diabetes-like syndrome was examined. In infected mice infiltration of mononuclear cells mixed with polymorphonuclear leuc...

  10. Effect of FTY720 and ICAM-1 mAb mono and combination therapy in cardiac allo-transplantation in rats

    Institute of Scientific and Technical Information of China (English)

    XIONG Hai-bo; HUANG Zu-fa; XIA Sui-sheng; YE Qi-fa; WEN Hao

    2005-01-01

    Objective To observe the effect of FTY720 and ICAM-1 mAb mono and combination therapy in cardiac silo-transplantation in rats. Methods Rats were randomly assigned to 9 groups, heart allo-transplantation were performed in abdominal site with micro-surgical technique. Recipients with allografts were treated with different doses of FTY720 and(or) ICAM-1 mAb. Graft survival, histopathology andlevel of serum IL-2, IFN-γ, IL-4, IL-10were investigated. Results Low doses of FTY720 (lmg/kg) combined with ICAM-1 mAb achieved synergistic effect in the prolongation of cardiac graft survival, combination index(CD =0.67. Conclusion Concomitant therapy of FTY720 and ICAM-1 mAb achieved a synergistic effect in the prolongation of heart allograft survival in rats.

  11. CHANGES OF CELLULAR ADHESION MOLECULES AND COMPLEMENT COMPONENT IN SERUM OF PATIENTS WITH UNSTABLE ANGINA%不稳定型心绞痛病人sCAMS与sC5b-9的变化

    Institute of Scientific and Technical Information of China (English)

    王立杰; 王红巧

    2011-01-01

    目的 探讨不稳定型心绞痛(UA)病人可溶性细胞黏附分子(sCAMS)与可溶性补体激活产物(sC5b-9)水平的变化及其意义.方法 采用ELISA方法 检测36例健康人和110例UA病人血清sCAMS、sC5b-9浓度的变化.结果 UA病人血清可溶性细胞间黏附分子-1(sICAM-1)、可溶性血管细胞间黏附分子-1(sVCAM-1)、sC5b-9浓度明显高于对照组,差异有极显著性(t=4.485~37.314,P<0.001);心绞痛发作时sICAM-1、sVCAM-1、sC5b-9的浓度增高较缓解后更明显(t=5.764~30.638,P<0.001);不同类型的心绞痛病人发作时和缓解后sICAM-1、sVCAM-1、sC5b-9浓度差异也有显著性(F=12.074~709.477,q=3.340~52.308,P<0.05~0.001);自发性心绞痛病人sCAMS、sC5b-9浓度增高较其他类型更明显.心绞痛发作时和缓解后,血清sC5b-9与sICAM-1、sVCAM-1浓度呈正相关(r=0.530~0.703,P<0.001).结论 UA的发生发展与CAMS和sC5b-9浓度变化有密切关系.%Objective To discuss the significance of changes of the levels of soluble cellular adhesion molecules (sCAMS) and complement activation component (sC5b-9) in patients with unstable angina (UA). Methods Using enzyme-linked immu-nosorbent assay (ELISA) , changes of serum levels of sCAMS and sC5b-9 were detected in 110 UA patients and 36 healthy people. Results Levels of soluble intercellular adhesion moleeule-1 (sICAM-1), soluble vascular cellular adhesion molecule-1 (sVCAM-1) and sC5b-9 in UA patients were significantly higher than that in healthy controls (t=4. 485 - 37. 314,P<0. 001) ; At angina pecto-ris attacks, the elevation of levels of sICAM-1, sVCAM-1 and sC5b-9 were more significant than after remission (2 = 5. 764 - 30. 638,P<0. 001). The differences of the above parameters in different type of patients at angina pectoris attacks and at remission were also significant (F=12. 074-709. 477;q=3. 340 - 52. 308;P<0. 05 - 0. 001), especially in those with spontaneous angina pectoris. The level of sC5b-9 was positively

  12. Clematichinenoside inhibits VCAM-1 and ICAM-1 expression in TNF-α-treated endothelial cells via NADPH oxidase-dependent IκB kinase/NF-κB pathway.

    Science.gov (United States)

    Yan, Simin; Zhang, Xu; Zheng, Haili; Hu, Danhong; Zhang, Yongtian; Guan, Qinghua; Liu, Lifang; Ding, Qilong; Li, Yunman

    2015-01-01

    Proinflammatory cytokine TNF-α-induced adhesion of leukocytes to endothelial cells plays a critical role in the early stage of atherosclerosis. Oxidative stress and redox-sensitive transcription factors are implicated in the process. Thus, compounds that mediate intracellular redox status and regulate transcription factors are of great therapeutic interest. Clematichinenoside (AR), a triterpene saponin isolated from the root of Clematis chinensis Osbeck, was previously demonstrated to have anti-inflammatory and antioxidative properties. However, little is known about the exact mechanism underlying these actions. Thus we performed a detailed study on its effect on leukocytes-endothelial cells adhesion with TNF-α-stimulated human umbilical vein endothelial cells (HUVECs) and cell-free systems. First, we found that AR reduced TNF-α-induced VCAM-1 and ICAM-1 expression and their promoter activity, inhibited translocation of p65 and phosphorylation of IκBα, suppressed IκB kinase-β (IKK-β) activity, lowered O2(∙-) and H2O2 levels, tackled p47(phox) translocation, and decreased NOX4 NADPH oxidase expression. Second, we showed that AR exhibited no direct free radical scavenging ability in cell-free systems at concentrations that were used in intact cells. Besides, AR had no direct effect on the activity of IKK-β that was extracted from TNF-α-stimulated HUVECs. We also found that p47 translocation, NOX4 expression, and reactive oxygen species (ROS) levels were up-regulated before IκB phosphorylation in TNF-α-induced HUVECs. Moreover, TNF-α-enhanced IKK-β activity was also inhibited by (polyethylene glycol) PEG-catalase, N-acetylcysteine (NAC), and vitamin E. In conclusion, these results suggest that AR reduces VCAM-1 and ICAM-1 expression through NADPH oxidase-dependent IKK/NF-κB pathways in TNF-α-induced HUVECs, which finally suppress monocyte-HUVECs adhesion. This compound is potentially beneficial for early-stage atherosclerosis. PMID:25463279

  13. NAC对体外循环血清致培养内皮细胞ICAM-1表达变化的影响%Effect of NAC on the changes of ICAM-1 expression induced by CPB serum on cultured endothelial cells

    Institute of Scientific and Technical Information of China (English)

    曾祥君; 肖颖彬; 王学锋

    2001-01-01

    目的 观察体外循环(CPB)血清对培养血管内皮细胞ICAM-1表达变化的影响,及N-乙酰半胱氨酸(NAC)的干预作用。方法 采用CPB血清致伤培养血管内皮细胞模型,以免疫组化方法观察培养血管内皮细胞ICAM-1表达量。结果 CPB血清可致培养血管内皮细胞ICAM-1表达量明显增加,NAC抑制培养内皮细胞ICAM-1的表达。结论 NAC可以抑制CPB血清所致的培养血管内皮细胞ICAM-1表达增加。因此NAC对体外循环后全身炎症反应可能有保护作用。%Objective To observe the effect of NAC on the changes of ICAM-1expression induced by CPB serum cultured endothelial cells. Methods ICAM-1 expression on cultured endothelial cells was detected by immunohistochemical techniques. Results ICAM-1 expression on cultured endothelial cells was increased by CPB serum, NAC inhibited ICAM-1 expression. Conclusion NAC could inhibit ICAM-1 expression on cultured endothelial cells, and might play a role in attenuating systemic inflammatory response syndrome induced by CPB.

  14. Signal regulatory protein alpha negatively regulates beta2 integrin-mediated monocyte adhesion, transendothelial migration and phagocytosis.

    Directory of Open Access Journals (Sweden)

    Dan-Qing Liu

    Full Text Available BACKGROUND: Signal regulate protein alpha (SIRPalpha is involved in many functional aspects of monocytes. Here we investigate the role of SIRPalpha in regulating beta(2 integrin-mediated monocyte adhesion, transendothelial migration (TEM and phagocytosis. METHODOLOGY/PRINCIPAL FINDINGS: THP-1 monocytes/macropahges treated with advanced glycation end products (AGEs resulted in a decrease of SIRPalpha expression but an increase of beta(2 integrin cell surface expression and beta(2 integrin-mediated adhesion to tumor necrosis factor-alpha (TNFalpha-stimulated human microvascular endothelial cell (HMEC-1 monolayers. In contrast, SIRPalpha overexpression in THP-1 cells showed a significant less monocyte chemotactic protein-1 (MCP-1-triggered cell surface expression of beta(2 integrins, in particular CD11b/CD18. SIRPalpha overexpression reduced beta(2 integrin-mediated firm adhesion of THP-1 cells to either TNFalpha-stimulated HMEC-1 monolayers or to immobilized intercellular adhesion molecule-1 (ICAM-1. SIRPalpha overexpression also reduced MCP-1-initiated migration of THP-1 cells across TNFalpha-stimulated HMEC-1 monolayers. Furthermore, beta(2 integrin-mediated THP-1 cell spreading and actin polymerization in response to MCP-1, and phagocytosis of bacteria were both inhibited by SIRPalpha overexpression. CONCLUSIONS/SIGNIFICANCE: SIRPalpha negatively regulates beta(2 integrin-mediated monocyte adhesion, transendothelial migration and phagocytosis, thus may serve as a critical molecule in preventing excessive activation and accumulation of monocytes in the arterial wall during early stage of atherosclerosis.

  15. ICAM-1在实验性大鼠肥厚心肌中的表达及真意义

    Institute of Scientific and Technical Information of China (English)

    谭晓; 王迪斌; 龙明智

    2004-01-01

    目的从转录和翻译两个水平研究细胞间粘附分子-1(ICAM-1)在大鼠肥厚心肌中的表达,探讨其与心肌肥厚的关系。方法取SD大鼠20只,随机分为2组,每组10只,1组为心肌肥厚组,2组为假手术组。分别测量心脏重量指数(Ponderal Index PI).应用免疫组织化学法检测ICAM-1及应用RT-PCR方法行ICAM-1 mRNA检测。结果心肌重量指数:肥厚组>假手术组;肥厚心肌中ICAM-1蛋白及ICAM-1mRNA表达明显增多。结论ICAM-1参与心肌肥厚的发生与发展。

  16. 未受控制的高血糖对2型糖尿病患者粘附分子的影响%Effect of uncontrolled hyperglycemia on levels of adhesion molecules in patients with diabetes mellitus type 2

    Institute of Scientific and Technical Information of China (English)

    Barbara RUSZKOWSKA-CIASTEK; Alina SOKUP; Tomasz WERNIK; Zofia RUPRECHT; Barbara GRALCZYK; Krzysztof GRALCZYK; Grayna GADOMSKA; Danuta RO

    2015-01-01

    目的:评估可溶性血管细胞间黏附分子(sVCAM-1)、可溶性细胞间黏附分子(sICAM-1)、可溶性选择素E和可溶性血栓调节蛋白在血糖控制良好和不受控制的2型糖尿病患者中的水平。  创新点:对2型糖尿病患者的血管内皮炎症标记物进行评估。  方法:62例糖尿病患者分成两组:第一组包括35个血糖控制良好的糖尿病患者,第二组包括27个未控制血糖并伴有微蛋白尿的糖尿病患者。对照组由25名健康志愿者组成。测定血浆中sVCAM-1、sICAM-1、可溶性选择素E和可溶性血栓调节蛋白的浓度,同时测定血清肌酐及血浆中空腹血糖和糖化血红蛋白(HbA1c)的浓度。  结论:与血糖控制良好的糖尿病组相比,未控制血糖组具有相对低的ICAM-1水平和更高的VCAM-1水平。未控制血糖组中患者的糖化血红蛋白和ICAM-1之间呈正相关,肾小球滤过率和可溶性选择素E之间呈正相关,而肌酐和ICAM-1之间呈负相关。研究证实2型糖尿病的发病机理中炎症过程的出现与血管内皮功能受损有关。未受控制的高血糖对粘附分子的反向作用表明,在糖尿病的并发症中VCAM-1和ICAM-1具有不同功能。%Objective: Uncontrol ed diabetes has become a major cause of mortality and morbidity by reason of vascular angiopathy. The aim of this study was to evaluate the concentrations of soluble forms of vascular adhesion molecule-1 (sVCAM-1), intercel ular adhesion molecule-1 (sICAM-1), E-selectin, and thrombomodulin in patients with wel-control ed and uncontrol ed diabetes type 2. Methods: The study was conducted on 62 patients with diabetes. Group I consisted of 35 patients with wel-control ed diabetes. The second group included 27 patients with uncontrol ed diabetes with micro-albuminuria. A control group was made up of 25 healthy volunteers. The concentrations of sVCAM-1, sICAM-1, sE-selectin, and soluble

  17. Troglitazone, a PPAR-γ activator prevents endothelial cell adhesion molecule expression and lymphocyte adhesion mediated by TNF-α

    Directory of Open Access Journals (Sweden)

    Itoh Makoto

    2005-02-01

    Full Text Available Abstract Background Cytokine mediated induction of the mucosal addressin cell adhesion molecule-1(MAdCAM-1 expression is associated with the onset and progression of inflammatory bowel disease (IBD. Results Using western blotting and cell-based ELISA, we show in this study that troglitazone, an activator of the peroxisome proliferator-activated receptor-γ (PPAR-γ, widely used in the treatment of diabetes, has as well recently been highlighted as protective in models of inflammation and cancer. We found that troglitazone (10–40 μM, significantly reduced the TNF-α (1 ng/ml mediated induction of endothelial MAdCAM-1 in a dose-dependent manner, achieving a 34.7% to 98.4% reduction in induced MAdCAM-1. Trogliazone (20μM reduced TNF-α induced VCAM-1, ICAM-1 and E-selectin expression. Moreover, troglitazone significantly reduced α4β7-integrin dependent lymphocyte adhesion to TNF-α cultured endothelial cells. Conclusions These results suggest that PPAR-γ agonists like troglitazone may be useful in the clinical treatment of IBD.

  18. Mechanism of sphingosine 1-phosphate- and lysophosphatidic Acid-induced up-regulation of adhesion molecules and eosinophil chemoattractant in nerve cells.

    LENUS (Irish Health Repository)

    Costello, Richard W

    2011-05-01

    The lysophospholipids sphingosine 1-phosphate (S1P) and lysophosphatidic acid (LPA) act via G-protein coupled receptors S1P(1-5) and LPA(1-3) respectively, and are implicated in allergy. Eosinophils accumulate at innervating cholinergic nerves in asthma and adhere to nerve cells via intercellular adhesion molecule-1 (ICAM-1). IMR-32 neuroblastoma cells were used as an in vitro cholinergic nerve cell model. The G(i) coupled receptors S1P(1), S1P(3), LPA(1), LPA(2) and LPA(3) were expressed on IMR-32 cells. Both S1P and LPA induced ERK phosphorylation and ERK- and G(i)-dependent up-regulation of ICAM-1 expression, with differing time courses. LPA also induced ERK- and G(i)-dependent up-regulation of the eosinophil chemoattractant, CCL-26. The eosinophil granule protein eosinophil peroxidase (EPO) induced ERK-dependent up-regulation of transcription of S1P(1), LPA(1), LPA(2) and LPA(3), providing the situation whereby eosinophil granule proteins may enhance S1P- and\\/or LPA- induced eosinophil accumulation at nerve cells in allergic conditions.

  19. Mechanism of sphingosine 1-phosphate- and lysophosphatidic Acid-induced up-regulation of adhesion molecules and eosinophil chemoattractant in nerve cells.

    LENUS (Irish Health Repository)

    Costello, Richard W

    2012-02-01

    The lysophospholipids sphingosine 1-phosphate (S1P) and lysophosphatidic acid (LPA) act via G-protein coupled receptors S1P(1-5) and LPA(1-3) respectively, and are implicated in allergy. Eosinophils accumulate at innervating cholinergic nerves in asthma and adhere to nerve cells via intercellular adhesion molecule-1 (ICAM-1). IMR-32 neuroblastoma cells were used as an in vitro cholinergic nerve cell model. The G(i) coupled receptors S1P(1), S1P(3), LPA(1), LPA(2) and LPA(3) were expressed on IMR-32 cells. Both S1P and LPA induced ERK phosphorylation and ERK- and G(i)-dependent up-regulation of ICAM-1 expression, with differing time courses. LPA also induced ERK- and G(i)-dependent up-regulation of the eosinophil chemoattractant, CCL-26. The eosinophil granule protein eosinophil peroxidase (EPO) induced ERK-dependent up-regulation of transcription of S1P(1), LPA(1), LPA(2) and LPA(3), providing the situation whereby eosinophil granule proteins may enhance S1P- and\\/or LPA- induced eosinophil accumulation at nerve cells in allergic conditions.

  20. Effects of isoflurane on ICAM-1 expression and neutrophils infiltration in rats with liver ischemia and reperfusion injury

    Institute of Scientific and Technical Information of China (English)

    Xu Guangmin; Tao Guocai

    2009-01-01

    Objective: To establish a rat model of warm partial hepatic ischemia-reperfusion (IR), and investigate the protective and anti-inflammatory effects of isoflurane on warm hepatic ischemia-reperfusion injury (IRI) in rats. Methods: Thirty-two female Sprague-Dawley rots were divided equally into 4 groups (n=8): PB-Sham group in which the rats were anesthetized by intraperitoneal injection of pentobarbital sodium (1.0%, 40 mg/kg, PB) and received a sham operation without occlusion of liver blood flow; PB-IR group whose rats underwent partial hepatic IR after anesthesia; Iso-Sham group in which inhalation of 1.0 MAC isoflurane and sham operation was performed; Iso-IR group in which 1.0 MAC isoflurane was inhaled for 4 h and IR was performed. Rat model of warm partial hepatic IR was established by clamping the hepatic arteries and hilar vessels distributing to the left and median lobes to induce partial hepatic ischemia (70%) for 60 min followed by reperfusion for 3 h. The rats were killed 3 h after declamping, and specimens of liver tissue and blood were obtained. The serum ALT and AST were detected as liver damage markers. Viability of myeloperoxidase (MPO) in liver was measured. The protein level of ICAM-1 in the liver was detected by immunohistochemistry and Western blotting. Results: Rats treated with 1.0 MAC isoflurane during warm partial (70%) hepatic ischemia 60 min and 3 h reperfusion had significantly lower serum ALT and AST compared with rats anesthetized with pentobarbital sodium subjected to hepatic IRI. The expression of ICAM-1 in hepatic tissue was significantly increased by hepatic IRI after pentobarbital sodium anesthesia. Isoflurane significantly inhibited protein expression of ICAM-1 in hepatic IR injury compared with pentobarbital sodium anesthesia. Viability of liver MPO was significantly increased by hepatic IRI after pentobarbital sodium anesthesia; Isoflurane can significantly inhibit MPO alteration in rat liver ischemia-reperfusion injury

  1. Budesonide and formoterol inhibit ICAM-1 and VCAM-1 expression of human lung fibroblasts

    NARCIS (Netherlands)

    Spoelstra, FM; Postma, DS; Hovenga, H; Noordhoek, JA; Kauffman, HF

    2000-01-01

    The glucocorticoid budesonide and the long-acting beta(2)-adrenoceptor agonist formoterol are used in asthma therapy for their anti-inflammatory and bronchodilating effects, respectively. Since expression of adhesion molecules on resident cells in the lung plays an important role in a