Circulation, Vol 89, 1511-1517, Copyright © 1994 by American Heart Association
MB Grant, TJ Wargovich, EA Ellis, S Caballero, M Mansour and CJ Pepine
In this study, we demonstrate, for the first time, the localization of
insulin-like growth factor I (IGF-I) in de novo and restenotic human
coronary atherectomy plaques by using immunocytochemical techniques. Smooth
muscle cells (SMCs) exhibiting the synthetic phenotype contained a
statistically significant higher concentration of IGF-I than SMCs of the
contractile phenotype or SMCs from normal coronary arteries. In addition,
we provide data to suggest that the long-acting somatostatin analogues
octreotide and angiopeptin inhibit IGF-I- and basic fibroblast growth
factor (b-FGF)- induced human coronary artery SMC proliferation.
Platelet-derived growth factor (PDGF)-stimulated cultures were minimally
affected by the addition of octreotide but were significantly inhibited by
angiopeptin. All three growth factors stimulated SMC migration in a
dose-dependent manner. The somatostatin analogues tested had no effect on
growth factor-stimulated SMC migration. Our data suggest that by reducing
SMC proliferation, somatostatin analogues may have clinical usefulness in
reducing the high incidence of restenosis observed after percutaneous
transluminal coronary artery interventions.
ARTICLES
Localization of insulin-like growth factor I and inhibition of coronary smooth muscle cell growth by somatostatin analogues in human coronary smooth muscle cells. A potential treatment for restenosis?
Division of Endocrinology, College of Medicine, University of Florida, Gainesville.
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