Open AccessGrowth Control and Morphogenesis in the Development and Pathology of Arteries
Author(s) -
Stephen M. Schwartz,
Lucy Liaw
Publication year - 1993
Publication title -
journal of cardiovascular pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.762
H-Index - 100
eISSN - 1533-4023
pISSN - 0160-2446
DOI - 10.1097/00005344-199321001-00007
Subject(s) - fibroblast growth factor , bradykinin , microbiology and biotechnology , growth factor , in vivo , endogeny , biology , morphogenesis , cell growth , vascular smooth muscle , endothelium , angiotensin ii , cell type , mechanism (biology) , endothelial stem cell , cell , smooth muscle , endocrinology , in vitro , receptor , biochemistry , philosophy , epistemology , gene , blood pressure
We briefly review and compare the current knowledge of growth mechanisms for the mitogenic response of endothelial cells and smooth-muscle cells to injury. For the endothelium, this focuses on the evidence that growth control involves two components: an endogenous inhibition mechanism, which can be overcome either by fibroblast growth factor (FGF) or by other agents that disrupt cell-cell junctions, and a separate mechanism, which requires FGF to allow cells to respond to a mitogenic effect. The smooth-muscle cell story is more complex; however, there is evidence here as well of an endogenous inhibitory mechanism, which may be overcome by a wide variety of agents. Platelet-derived growth factor, long seen as a major mitogen, does not itself now appear to be a major mitogen in vivo. In contrast, FGF also seems to play a major role in initiating smooth-muscle replication. Other molecules, including angiotensin II, bradykinin, thrombin, and catecholamines, are beginning to appear to play major roles in control of smooth-muscle replication in vivo as well.