Circulation, Vol 72, 735-740, Copyright © 1985 by American Heart Association
DF Bowen-Pope, R Ross and RA Seifert
Release of platelet-derived growth factor (PDGF) from platelets has been
postulated to stimulate at least some of the cell proliferation seen at
sites of tissue damage, both beneficially (wound healing) and perniciously
(during formation of atherosclerotic lesions). Two other growth factors
have been localized to the platelet: epidermal growth factor and
transforming growth factor. These factors may function synergistically with
PDGF in promoting smooth muscle cell proliferation in the injured vessel
wall. PDGF-like molecules (PDGF-c) that bind to the PDGF receptor and are
at least partially recognized by antiserum against PDGF may also be
synthesized by vessel wall cells themselves under certain circumstances.
Arterial endothelial cells secrete several mitogens, one of which is a
PDGF-c. Release is greatly stimulated by exposure of the cells to
physiologic concentrations of thrombin. Also, aortic smooth muscle cells
from 2-week-old rats secrete mitogenic levels of PDGF-c. In this case,
PDGF-c accounts for all the mitogenic activity in conditioned medium (when
assayed on 3T3 cells). Smooth muscle cells obtained from adult rat aortae
secrete 150-fold less PDGF- c. In a third example, when adult rat carotid
arteries are damaged with a balloon catheter, smooth muscle cells migrate
into the intima of the artery and proliferate. By 2 weeks, the number of
smooth muscle cells in the artery has doubled. When these intimal smooth
muscle cells are cultured, they are found to secrete PDGF-c. These findings
suggest that activation of endogenous synthesis of PDGF-c may contribute to
the smooth muscle cell proliferation seen in response to vascular injury.
ARTICLES
Locally acting growth factors for vascular smooth muscle cells: endogenous synthesis and release from platelets
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