scholarly journals Transforming Growth Factor-β and Receptor Tyrosine Kinase–Activating Growth Factors Negatively Regulate Collagen Genes in Smooth Muscle of Hypertensive Rats

Hypertension ◽  
1998 ◽  
Vol 31 (4) ◽  
pp. 986-994 ◽  
Author(s):  
Paula Bray ◽  
Alex Agrotis ◽  
Alex Bobik
Keyword(s):  
Smooth Muscle ◽  
Growth Factors ◽  
Growth Factor ◽  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Hypertensive Rats ◽  
Collagen Genes

scholarly journals Effects of Cyclic Strain and Growth Factors on Vascular Smooth Muscle Cell Responses

2009 ◽  
Vol 3 (1) ◽  
pp. 28-38 ◽  
Author(s):  
Soujanya Kona ◽  
Prithiviraj Chellamuthu ◽  
Hao Xu ◽  
Seth R Hills ◽  
Kytai Truong Nguyen
Keyword(s):  
Smooth Muscle ◽  
Growth Factors ◽  
Growth Factor ◽  
Vascular Smooth Muscle ◽  
Transforming Growth Factor ◽  
Growth Factor Receptor ◽  
Cyclic Strain ◽  
Transforming Growth Factor Β ◽  
Positive Influence ◽  
Biomechanical Forces

Under physiological and pathological conditions, vascular smooth muscle cells (SMC) are exposed to different biochemical factors and biomechanical forces. Previous studies pertaining to SMC responses have not investigated the effects of both factors on SMCs. Thus, in our research we investigated the combined effects of growth factors like Bfgf (basic fibroblast growth factor), TGF-β (transforming growth factor β) and PDGF (platelet-derived growth factor) along with physiological cyclic strain on SMC responses. Physiological cyclic strain (10% strain) significantly reduced SMC proliferation compared to static controls while addition of growth factors bFGF, TGF-β or PDGF-AB had a positive influence on SMC growth compared to strain alone. Microarray analysis of SMCs exposed to these growth factors and cyclic strain showed that several bioactive genes (vascular endothelial growth factor, epidermal growth factor receptor, etc.) were altered upon exposure. Further work involving biochemical and pathological cyclic strain stimulation will help us better understand the role of cyclic strain and growth factors in vascular functions and development of vascular disorders.

scholarly journals Proxy activation of protein ErbB2 by heterologous ligands implies a heterotetrameric mode of receptor tyrosine kinase interaction

1998 ◽  
Vol 331 (1) ◽  
pp. 113-119 ◽  
Author(s):  
Guo Cai HUANG ◽  
Xiaomei OUYANG ◽  
Richard J. EPSTEIN
Keyword(s):  
Growth Factor ◽  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Epidermal Growth Factor Receptors ◽  
Type I ◽  
A431 Cells ◽  
Erbb2 Receptor ◽  
Epidermal Growth

The oncoprotein ErbB2 is frequently overexpressed in human tumours, but no activating ErbB2-specific ligand has yet been identified. Here we analyse the catalytic and oligomeric behaviour of ErbB2 using phosphorylation-state-specific antibodies which distinguish kinase-active and -inactive ErbB2 receptor subsets. Heregulin-α (HRG) activates ErbB2 in G8/DHFR 3T3 cells by selectively inducing hetero-oligomerization with kinase-defective ErbB3, indicating that heterologous transphosphorylation is an unlikely prerequisite for ErbB2 activation. HRG also triggers association of epidermal-growth-factor receptors (EGFR) with a kinase-inactive ErbB2 subset while reducing EGFR association with active ErbB2. Similarly, EGF treatment of A431 cells induces concomitant hetero-oligomerization of active ErbB2 with inactive EGFR, of active EGFR with inactive ErbB2, and of inactive ErbB2 with kinase-defective ErbB3. These combinatorial patterns of ligand-dependent oligomerization suggest a multivalent model of receptor tyrosine kinase interaction in which liganded homodimers provide stable oligomerization interfaces for unliganded ErbB2 or other bystander receptors. We submit that ErbB2 may be physiologically activated via a ‘proxy ’ ligand-inducible heterotetrameric mechanism similar to that already established for transforming-growth-factor-β type I receptors.

Metalloproteinase and growth factor interactions: do they play a role in pulmonary fibrosis?

2002 ◽  
Vol 283 (1) ◽  
pp. L1-L11 ◽  
Author(s):  
Margaret K. Winkler ◽  
John L. Fowlkes
Keyword(s):  
Acute Lung Injury ◽  
Growth Factors ◽  
Growth Factor ◽  
Pulmonary Fibrosis ◽  
Lung Injury ◽  
Transforming Growth Factor ◽  
Interstitial Fibrosis ◽  
Inflammatory Cells ◽  
Transforming Growth Factor Β ◽  
Target Cells

Chronic lung disease due to interstitial fibrosis can be a consequence of acute lung injury and inflammation. The inflammatory response is mediated through the migration of inflammatory cells, actions of proinflammatory cytokines, and the secretion of matrix-degrading proteinases. After the initial inflammatory insult, successful healing of the lung may occur, or alternatively, dysregulated tissue repair can result in scarring and fibrosis. On the basis of recent insights into the mechanisms underlying acute lung injury and its long-term consequences, data suggest that proteinases, such as the matrix metalloproteinases (MMPs), may not only be involved in the breakdown and remodeling that occurs during the injury but may also cause the release of growth factors and cytokines known to influence growth and differentiation of target cells within the lung. Through the release of and activation of fibrosis-promoting cytokines and growth factors such as transforming growth factor-β1, tumor necrosis factor-α, and insulin-like growth factors by MMPs, we propose that these metalloproteinases may be integral to the initiation and progression of pulmonary fibrosis.

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