Transforming Growth Factor-Beta Inhibits Heme Oxygenase-1 Expression in Lung Fibroblasts through Nuclear Factor-Kappa-B-Dependent Pathway

Pharmacology ◽  
2014 ◽  
Vol 93 (3-4) ◽  
pp. 185-192 ◽  
Author(s):  
Ying Xie ◽  
Ye Wang ◽  
Chuanyue Zong ◽  
Jiawen Cheng
Keyword(s):  
Growth Factor ◽  
Heme Oxygenase ◽  
Transforming Growth Factor Beta ◽  
Nuclear Factor Kappa B ◽  
Transforming Growth Factor ◽  
Lung Fibroblasts ◽  
Heme Oxygenase 1 ◽  
Nuclear Factor ◽  
Growth Factor Beta ◽  
Dependent Pathway

Cellular and molecular mechanisms of chronic rhinosinusitis and potential therapeutic strategies: review on cytokines, nuclear factor kappa B and transforming growth factor beta

2015 ◽  
Vol 129 (S3) ◽  
pp. S2-S7 ◽  
Author(s):  
N T Phan ◽  
P J Cabot ◽  
B D Wallwork ◽  
A U Cervin ◽  
B J Panizza
Keyword(s):  
Growth Factor ◽  
Chronic Rhinosinusitis ◽  
Transforming Growth Factor Beta ◽  
Nuclear Factor Kappa B ◽  
Transforming Growth Factor ◽  
Therapeutic Strategies ◽  
Nuclear Factor ◽  
T Helper ◽  
Nuclear Factor Kappa ◽  
Growth Factor Beta

AbstractBackground:Chronic rhinosinusitis is characterised by persistent inflammation of the sinonasal mucosa. Multiple pathophysiological mechanisms are likely to exist. Previous research has focused predominantly on T-helper type cytokines to highlight the inflammatory mechanisms. However, proteins such as nuclear factor kappa B and transforming growth factor beta are increasingly recognised to have important roles in sinonasal inflammation and tissue remodelling.Objective:This review article explores the roles of T-helper type cytokines, nuclear factor kappa B and transforming growth factor beta in the pathophysiological mechanisms of chronic rhinosinusitis. An understanding of these mechanisms will allow for better identification and classification of chronic rhinosinusitis endotypes, and, ultimately, improved therapeutic strategies.

scholarly journals Transforming Growth Factor Beta 2 and Heme Oxygenase 1 Genes Are Risk Factors for the Cerebral Malaria Syndrome in Angolan Children

PLoS ONE ◽  
2010 ◽  
Vol 5 (6) ◽  
pp. e11141 ◽  
Author(s):  
Maria Rosário Sambo ◽  
Maria Jesus Trovoada ◽  
Carla Benchimol ◽  
Vatúsia Quinhentos ◽  
Lígia Gonçalves ◽  
...  
Keyword(s):  
Risk Factors ◽  
Growth Factor ◽  
Cerebral Malaria ◽  
Heme Oxygenase ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Heme Oxygenase 1 ◽  
Growth Factor Beta ◽  
Beta 2

Cytokine signaling in lung: transforming growth factor-beta secretion by lung fibroblasts

1991 ◽  
Vol 260 (2) ◽  
pp. L123-L128 ◽  
Author(s):  
J. Kelley ◽  
J. P. Fabisiak ◽  
K. Hawes ◽  
M. Absher
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Phenotypic Expression ◽  
Soft Agar ◽  
Lung Fibroblast ◽  
Lung Fibroblasts ◽  
Tgf Beta ◽  
Anchorage Independent Growth ◽  
Growth Factor Beta

Control of growth and phenotypic expression of interstitial fibroblasts is a critical determinant of lung architecture and physiology during processes of growth and remodeling. We examined the ability of lung fibroblasts to produce transforming growth factor-beta (TGF-beta), a cytokine that is known to modulate proliferation and phenotypic expression of mesenchymal cells. Cultures of fibroblasts isolated from rat lungs spontaneously secrete TGF-beta as measured in the standard bioassay of anchorage-independent growth of normal rat kidney (NRK) cells in soft agar. Rat lung fibroblasts secrete TGF-beta in an inactive precursor form. Fibroblasts cultured from adult and fetal rat lungs produced comparable amounts of TGF-beta. The ability of lung fibroblast supernatant fluids to induce colony formation in soft agar could be completely neutralized by preincubation of samples with anti-TGF-beta immunoglobulin (Ig). Anti-platelet-derived growth factor IgG had no effect on anchorage-independent growth of NRK cells driven by rat fibroblast culture supernatant samples. These results indicate that TGF-beta does not require the presence of and interaction with secondary cytokines for its activity. In contrast to the results obtained with rat cells, neither human fetal nor adult lung fibroblasts secreted detectable amount of active TGF-beta or its inactive precursor. This was not due to the presence of TGF-beta inhibitors in fibroblast culture media, because the addition of purified porcine TGF-beta to conditioned medium from human lung fibroblast cultures yielded the expected increase in NRK cell growth in soft agar. These results point to differing cytokine control patterns in the lungs of the two species.

scholarly journals Enhanced production and extracellular deposition of the endothelial-type plasminogen activator inhibitor in cultured human lung fibroblasts by transforming growth factor-beta.

1986 ◽  
Vol 103 (6) ◽  
pp. 2403-2410 ◽  
Author(s):  
M Laiho ◽  
O Saksela ◽  
P A Andreasen ◽  
J Keski-Oja
Keyword(s):  
Growth Factor ◽  
Plasminogen Activator ◽  
Transforming Growth Factor Beta ◽  
Culture Medium ◽  
Transforming Growth Factor ◽  
Lung Fibroblasts ◽  
Tissue Type ◽  
Metabolic Labeling ◽  
Tgf Beta ◽  
Growth Factor Beta

Cultured human embryonic lung fibroblasts were used as a model to study the effects of transforming growth factor-beta (TGF beta) on the plasminogen activator (PA) activity released by nontumorigenic cells into the culture medium. The cells were exposed to TGF beta under serum-free conditions, and the changes in PA activity and protein metabolism were analyzed by caseinolysis-in-agar assays, zymography, and polypeptide analysis. Treatment of the cells with TGF beta caused a significant decrease in the PA activity of the culture medium as analyzed by the caseinolysis-in-agar assays. The quantitatively most prominent effect of TGF beta on confluent cultures of cells was the induction of an Mr 47,000 protein, as detected by metabolic labeling. The Mr 47,000 protein was a PA inhibitor as judged by reverse zymography. It was antigenically related to a PA inhibitor secreted by HT-1080 tumor cells as demonstrated with monoclonal antibodies. The induced Mr 47,000 inhibitor was deposited into the growth substratum of the cells, as detected by metabolic labeling, immunoblotting analysis, and reverse zymography assays of extracellular matrix preparations. TGF beta also decreased the amounts of urokinase-type and tissue-type PAs accumulated in the conditioned medium, as detected by zymography. Epidermal growth factor antagonized the inhibitory effects of TGF beta by enhancing the amounts of the PAs. These results indicate that growth factors modulate the proteolytic balance of cultured cells by altering the amounts of PAs and their inhibitors.

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