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J. Biol. Chem., Vol. 277, Issue 39, 36338-36344, September 27, 2002
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From the Diabetes causes accelerated atherosclerosis and
subsequent cardiovascular disease through mechanisms that are poorly
understood. We have previously shown, using a porcine model of
diabetes-accelerated atherosclerosis, that diabetes leads to an
increased accumulation and proliferation of arterial smooth muscle
cells in atherosclerotic lesions and that this is associated with
elevated levels of plasma triglycerides. We therefore used the same
model to investigate the mechanism whereby diabetes may stimulate
smooth muscle cell proliferation. We show that lesions from diabetic
pigs fed a cholesterol-rich diet contain abundant insulin-like growth
factor-I (IGF-I), in contrast to lesions from non-diabetic pigs.
Furthermore, two fatty acids common in triglycerides, oleate and
linoleate, enhance the growth-promoting effects of IGF-I in smooth
muscle cells isolated from these animals. These fatty acids accumulate
predominantly in the membrane phospholipid pool; oleate accumulates
preferentially in phosphatidylcholine and
phosphatidylethanolamine, whereas linoleate is found mainly in
phosphatidylethanolamine. The growth-promoting effects of
oleate and linoleate depend on phospholipid hydrolysis by phospholipase
D and subsequent generation of diacylglycerol. Thus, concurrent
increases in levels of IGF-I and triglyceride-derived oleate and
linoleate in lesions may contribute to accumulation and proliferation
of smooth muscle cells and lesion progression in diabetes-accelerated atherosclerosis.
Oleate and Linoleate Enhance the Growth-promoting Effects of
Insulin-like Growth Factor-I through a Phospholipase
D-dependent Pathway in Arterial Smooth Muscle Cells*
§,,
, and**
Department of Pathology, University of
Washington School of Medicine, Seattle, Washington 98195, ¶ Department of Pharmacology, New York Medical College, Valhalla,
New York 10595, and Department of Pathology, Medical College of
Georgia, Augusta, Georgia 30912
*
These studies were supported in part by National Institutes
of Health Grants HL62887 (to K. B.), HL34300 and HL25394 (to M. C.),
and HL55798 (to R. G.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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