Hypertension, Vol 23, 593-599, Copyright © 1994 by American Heart Association
A Agrotis, J Saltis and A Bobik
Cultured vascular smooth muscle cells derived from the spontaneously
hypertensive rat (SHR) are known to replicate more rapidly than cells from
the normotensive Wistar-Kyoto (WKY) rat. In this study we compared the
responses of vascular smooth muscle cells from the two strains to
transforming growth factor-beta 1 (TGF-beta 1) and evaluated its potential
to account for the different growth properties of these cells in response
to a number of vascular-derived growth factors. TGF-beta 1 potentiated the
proliferative effects of epidermal growth factor, basic fibroblast growth
factor, or the different isoforms of platelet-derived growth factor on
vascular smooth muscle cells from SHR but inhibited growth
factor-stimulated proliferation of vascular smooth muscle cells from WKY
rats. These differential effects of TGF-beta 1 on proliferation could not
be attributed to alterations in the expression of the type I, II, or III
TGF-beta receptors but appeared more related to the ability of cells to
autoinduce the TGF-beta 1 gene. TGF-beta 1 caused a time-dependent increase
in its own mRNA levels in vascular smooth muscle cells of WKY rats but
attenuated levels in vascular smooth muscle cells of SHR. This effect was
specific to TGF-beta 1 autoinduction since similar elevations in TGF-beta 1
mRNA levels were observed when vascular smooth muscle cells from the two
rat strains were exposed to phorbol myristate acetate, basic fibroblast
growth factor, or platelet-derived growth factor-BB.(ABSTRACT TRUNCATED AT
250 WORDS)
ARTICLES
Transforming growth factor-beta 1 gene activation and growth of smooth muscle from hypertensive rats
Baker Medical Research Institute, Prahran, Victoria, Australia.
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