factor-beta hypoxia-inducible factor-1alpha: Topics by WorldWideScience.org

c-Myc Mediates a Hypoxia-Induced Decrease in Acetylated Histone H4

Hypoxia inducible factor-1 (HIF-1) promotes tumor cell adaptation to microenvironmental stress. HIF-1 is up-regulated in irradiated tumors and serves as a promising target for radiosensitization....Full Text Available

2009-04-01

SirT3 suppresses hypoxia inducible factor 1? and tumor growth by inhibiting mitochondrial ROS production

Global acetylation of histone H4 is a mark of gene transcriptional activation. The c-Myc transcription factor binds to specific DNA sites in cellular chromatin and induces the acetylation of...Full Text Available

2009-10-01

Regulation of life span by mitochondrial respiration: the HIF-1 and ROS connection

It has become increasing clear that alterations in cellular metabolism have a key role in the generation and maintenance of cancer. Some of the metabolic changes can be attributed to the activation...Full Text Available

2011-06-30

Pretreatment with a soluble activin type IIB receptor/Fc fusion protein improves hypoxia-induced muscle dysfunction

A mild reduction in mitochondrial respiration extends the life span of many species, including C. elegans. We recently showed that hypoxia-inducible factor 1 (HIF-1) is required for...Full Text Available

Glucocorticoids exacerbate hypoxia induced expression of the pro-apoptotic gene Bnip3 in the developing cortex

Hypoxia, or reduced oxygen, occurs in a variety of clinical and environmental situations. Hypoxic exposure is associated with decreased muscle mass and a concomitant reduction in exercise capacity,...Full Text Available

2010-01-01

Duplication and Diversification of the Hypoxia-Inducible IGFBP-1 Gene in Zebrafish

Neonatal administration of the synthetic glucocorticoid, dexamethasone (DEX) retards brain growth, alters adult behaviors and induces cell death in the rat brain, thereby implicating glucocorticoids...Full Text Available

2007-01-19

Adenomatous Polyposis Coli and Hypoxia-inducible Factor-1? Have an Antagonistic Connection

BackgroundGene duplication is the primary force of new gene evolution. Deciphering whether a pair of duplicated genes has evolved divergent functions is often challenging. The zebrafish...Full Text Available

Transforming growth factor-? signaling mediates hypoxia-induced pulmonary arterial remodeling and inhibition of alveolar development in newborn mouse lung

The tumor suppressor adenomatous polyposis coli (APC) is mutated in the majority of colorectal cancers and is best known for its role as a scaffold in a Wnt-regulated protein complex that determines...Full Text Available

2010-11-01

The Function of Hypoxia-Inducible Factor (HIF) Is Independent of the Endoplasmic Reticulum Protein OS-9

Hypoxia causes abnormal neonatal pulmonary artery remodeling (PAR) and inhibition of alveolar development (IAD). Transforming growth factor (TGF)-β is an important regulator of lung development...Full Text Available

2008-07-01

NADPH oxidase-mediated reactive oxygen species production activates hypoxia-inducible factor-1 (HIF-1) via the ERK pathway after hyperthermia treatment

The protein “amplified in osteosarcoma-9” (OS-9) has been shown previously to interact with the prolyl hydroxylases PHD2 and PHD3. These enzymes initiate oxygen-dependent degradation...Full Text Available

Changes of hypoxia inducible factor-1 ? in hepatoma cells irradiated by gamma ray and their mechanism

Hyperthermia (HT) is a strong adjuvant treatment with radiotherapy and chemotherapy because it causes tumor reoxygenation. However, the detailed molecular mechanisms of how HT enhances tumor oxygenation...Full Text Available

2010-11-23

Regulation of Redd1 Expression by Hypoxia

This paper reports regulation of hypoxia inducible factor-1 ? (HIF-1 ?)in hepatoma cells by irradiation. Cobalt chloride (CoCl2), a chemical mimic agent for hypoxia research, was utilized to induce the stable expression of HIF-1 ? in HepG2 cells. The HepG2 cells were irradiated to different doses to observe the changes of HIF-1 ?. The level of intracellular reactive oxygen species (ROS) was assayed by fluorescent microscope and flow cytometry (FCM). The results showed that there were obvious changes in expression of HIF-1 ? after HepG2 cells exposed to radiation, and the changes were positively related with the irradiation dose from 1 Gy to 5 Gy. Moreover, contents of incellular ROS were negatively correlated with above levels of HIF-1 ? from 1 Gy to 3 Gy. The results indicate that irradiation may enhance hypoxic cells HIF-1 ?, and the reduction of intracellular ROS can contribute to the regulation of ionizing radiation on HIF-1 ?. (authors)

2007-10-01

Type I (RI) and type II (RII) receptors for transforming growth factor-beta isoforms are expressed subsequent to transforming growth factor-beta ligands during excisional wound repair.

Redd1, a recently discovered stress-response gene, is regulated by hypoxia via hypoxia-inducible factor 1 (HIF-1) and by DNA damage via p53/p63; however, the signaling pathway by which its expression is induced by hypoxia has not been elucidated. We demonstrated that the up-regulation of Redd1 transcription by hypoxia and high cell density (HCD) depends on cooperation between Sp1 and HIF-1#alpha# downstream of the PI3K/Akt pathway.

2006-05-25

Mechanisms of obesity-induced male infertility

Transforming growth factor (TGF)-beta isoforms (TGF-beta 1, -beta 2, and -beta 3) regulate cell growth and differentiation and have critical regulatory roles in the process of tissue repair and remodeling....Full Text Available

1997-01-01

British Library Electronic Table of Contents (United Kingdom)

Male infertility, characterized by hypogonadism, decreased semen quality or ejaculatory dysfunction, accounts for approximately 20% of infertility cases. Obesity and metabolic dysfunction have been identified, among other causal factors, to contribute to male infertility. In the context of the Western world's `obesity epidemic', this article discusses three main biological mechanisms linking obesity to impaired male reproductive function: hypogonadism, testicular heat stress/hypoxia-induced apoptosis and endocrine disruption by `obesogens'. Among these, obesity-induced hypogonadism is undoubtedly the most clinically significant and is easily assessed. Rapidly expanding areas of research in this area include leptin modulation of kisspeptins and hypothalamic-pituitary-testicular hormone path...

2010-01-01

Transforming growth factor-beta signaling in thoracic aortic aneurysm development: a paradox in pathogenesis

Transforming Growth Factor Beta One (TGF-?1) Enhancement of the Chondrocytic Phenotype in Aged Perichondrial Cells

Thoracic aortic aneurysms (TAAs) are potentially devastating, and due to their asymptomatic behavior, pose a serious health risk characterized by the lack of medical treatment options and high...Full Text Available

2009-01-01

Preclinical evidence for the benefits of penile rehabilitation therapy following nerve-sparing radical prostatectomy.

BackgroundPerichondrium is recognized as a tissue with chondrogenic potential yielding cells which can be used for osteochondral repair. Factors which influence the proliferative...Full Text Available

2000-01-01

Science.gov (United States)

Erectile dysfunction following radical prostatectomy remains a frequent problem despite the development of nerve-sparing techniques. This erectile dysfunction is believed to be neurogenic, enhanced by hypoxia-induced structural changes which result in additional veno-occlusive dysfunction. Recently, daily use of intracavernous vasoactive substances and oral use of PDE5-inhibitors have been clinically studied for treatment of postprostatectomy erectile dysfunction. Since these studies showed benefits of "penile rehabilitation therapy," these effects have been studied in a preclinical setting. We reviewed experimental literature on erectile tissue preserving and neuroregenerative treatment strategies, and found that preservation of the erectile tissue by the use of intracavernous nitric oxide donors or vasoactive substances, oral PDE5-inhibitors, and hyperbaric oxygen therapy improved erectile function by antifibrotic effects and preservation of smooth muscle. ...

2008-01-01

Different phenotypes of lattice corneal dystrophy type I in patients with 417C>T (R124C) and 1762A>G (H572R) mutations in TGFBI (BIGH3)

Computerized tomography-guided neurolytic splanchnic nerve block

PurposeTo describe clinical data and to characterize mutations in the transforming growth factor beta-induced (TGFBI) gene in patients from three unrelated Chilean...Full Text Available

TGF-@b/BMPs: Crucial crossroad in neural autoimmune disorders

Computerized tomography-guided neurolytic splanchnic nerve block is a technique for relieving abdominal cancer pain; the goal is the alcoholic neurolytic interruption of the sensitive structures in retroperitoneal space. Computerized tomography yields accurate anatomical detailing and the course for needle placement and alcohol spread. January, 1993, to July, 1996, twenty-one bilateral splanchnic nerve blocks were performed through the posterior access. Forty-eight hours after alcoholism. 14 patients (66%) had complete pain regression; 52% of the patients needed no analgesics for 6 to 54 days and only 9 patients (42%) needed another low opioid therapy. Complications included hypotension and diarrhea in all cases. One had a cardiac arrest and diet 8 days after the procedure. There were no other complications. The whole procedure usually lasted 60 min (range: 45 to 90 min). Splanchnic nerve neurolysis is a useful treatment in the patients with severe chronic abdominal pain. It is used as ...

1997-01-01

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British Library Electronic Table of Contents (United Kingdom)

Transforming growth factor beta (TGF-@b) has a crucial role in the differentiation of ectodermal cells to neural or epidermal precursors. TGF-@b and bone morphogenetic protein molecules (BMPs) are involved in many developmental processes, including cell proliferation and differentiation, apoptosis, mitotic arrest and intercellular interactions during morphogenesis. Additionally, the failure of central thymic tolerance mechanisms, leading to T cells with a skewed autoreactive response, is being described as a contributor in inflammatory processes in autoimmune diseases such as multiple sclerosis. Since TGF-@b and BMP proteins are crucial for the development of the neural system and the thymus, as well as for the differentiation of T cells, it is essential to further investigate their role i...

2011-01-01

Effect of transforming growth factor beta on synthesis of glycosaminoglycans by human lung fibroblasts

The structure of myostatin:follistatin 288: insights into receptor utilization and heparin binding

The processes of lung growth, injury, and repair are characterized by alterations in fibroblast synthesis and interstitial distribution of extracellular matrix components. Transforming growth factor beta (TGF-beta), which is postulated to play a role in modulating lung repair, alters the distribution of several matrix components such as collagen and fibronectin. We studied the effect of TGF-beta on the synthesis and distribution of the various glycosaminoglycans (GAGs) and whether these effects may explain its role in lung repair. Human diploid lung fibroblasts (IMR-90) were exposed to various concentrations of TGF-beta (0-5 nM) for variable periods of time (0-18 h). Newly synthesized GAGs were labeled with either (3H)glucosamine or (35S)sulfate. Individual GAGs were separated by size exclusion chromatography after serial enzymatic and chemical digestions and quantitated using scintillation counting. There was a dose-dependent increase in total ...

1990-09-01

Science.gov (United States)

Myostatin is a member of the transforming growth factor-{beta} (TGF-{beta}) family and a strong negative regulator of muscle growth. Here, we present the crystal structure of myostatin in complex with the antagonist follistatin 288 (Fst288). We find that the prehelix region of myostatin very closely resembles that of TGF-{beta} class members and that this region alone can be swapped into activin A to confer signalling through the non-canonical type I receptor Alk5. Furthermore, the N-terminal domain of Fst288 undergoes conformational rearrangements to bind myostatin and likely acts as a site of specificity for the antagonist. In addition, a unique continuous electropositive surface is created when myostatin binds Fst288, which significantly increases the affinity for heparin. This translates into stronger interactions with the cell surface and enhanced myostatin degradation in the presence of either Fst288 or Fst315. Overall, we have identified several ...

2009-09-29

The effects of surface damage on RF cavity operation

Angiogenic cytokines and growth factors in systemic sclerosis.

We describe a model of damage in rf cavities and show how this damage can limit cavity operation. We first present a review of mechanisms that may or may not affect the ultimate fields that can be obtained in rf cavities, assuming that mechanical stress explains the triggers of rf breakdown events. We present a method of quantifying the surface damage caused by breakdown events in terms of the spectrum of field enhancement factors, Beta, for asperities on the surface. We then model an equilibrium that can develop between damage and conditioning effects, and show how this equilibrium can determine cavity performance and show experimental evidence for this mechanism. We define three functions that quantify damage, and explain how the parameters that determine this performance can be factored out and measured. We then show how this model can quantitatively explain the dependence of cavity performance on material, frequency, pulse length, gas, ...

2006-04-14

Science.gov (United States)

Systemic sclerosis is an autoimmune connective tissue disorder characterized by a widespread microangiopathy, autoimmunity and fibrosis of the skin and of various internal organs. Microangiopathy is characterized by a reduced capillary density and an irregular chaotic architecture that lead to chronic tissue hypoxia. Despite the hypoxic conditions, there is no evidence for a sufficient compensative angiogenesis in SSc. Furthermore, vasculogenesis is also impaired. An imbalance between angiogenic and angiostatic factors might explain the pathogenetic mechanisms of SSc vasculopathy. As far as angiogenic factors are concerned, within the most important are vascular endothelial growth factor (VEGF) and its receptors, platelet derived growth factor (PDGF), transforming growth factor beta (TGF-?), fibroblast growth factor -2 (FGF-2), angiopoietin 1 (Ang-1), stromal cell-derived factor 1 (SDF-1/CXCL12), endothelin-1 (ET-1), monocyte chemoattractant ...

2011-04-28

Proteomic Profiling of Mesenchymal Stem Cell Responses to Mechanical Strain and TGF-B1

Inhibitory effect of transforming growth factor-. beta. (TGF-. beta. ) on insulin-like growth factor 1 (IGF-1)-induced proliferation and differentiation in primary cultures of pig preadipocytes

Mesenchymal stem cells (MSCs) are a potential source of smooth muscle cells (SMCs) for constructing tissue-engineered vascular grafts. However, the details of how specific combinations of vascular microenvironmental factors regulate MSCs are not well understood. Previous studies have suggested that both mechanical stimulation with uniaxial cyclic strain and chemical stimulation with transforming growth factor {beta}1 (TGF-{beta}1) can induce smooth muscle markers in MSCs. In this study, we investigated the combined effects of uniaxial cyclic strain and TGF-{beta}1 stimulation on MSCs. By using a proteomic analysis, we found differential regulation of several proteins and genes, such as the up-regulation of TGF-{beta}1-induced protein ig-h3 (BGH3) protein levels by TGF-{beta}1 and up-regulation of calponin 3 protein level by cyclic strain. At the gene expression level, BGH3 was induced by TGF-{beta}1, but calponin 3 was not significantly ...

2009-10-12

Inhibitory effect of transforming growth factor-#beta# (TGF-#beta#) on insulin-like growth factor 1 (IGF-1)-induced proliferation and differentiation in primary cultures of pig preadipocytes

The influence of serum, IGF-1 and TGF-{beta} on the differentiation of preadipocytes was examined in primary cultures of porcine adipose tissue cells. In serum-supplemented or serum-free, IGF-1 (1 and 10 nM) had no effect on total cell number. However, IGF-1 (10nM) increased adipocyte number only in serum-supplemented (1% pig serum) cultures, whereas TGF-{beta} (15 pm) reduced the adipocyte number in the presence and absence of IGF-1. Replication of preadipocytes was analyzed with a ({sup 3}H) thymidine assay. Preadipocyte proliferation (cpm in adipocyte fraction) was increased by IGF-1 (10nM) only in cultures containing pig serum. TGF-{beta} had no effect on preadipocyte proliferation specifically, but slightly increased total ({sup 3}H) thymidine incorporation in cultures with serum. Glycerol phosphate dehydrogenase (GPDH) specific activity was decreased by adding TGF-{beta} to serum-free cultures but TGF-{beta} had little effect in serum-supplemented cultures. Cellular secretion of ...

1990-02-26