(Circulation. 2000;101:1311.)
© 2000 American Heart Association, Inc.
Basic Science Reports |
Expression and Function of PPAR
in Rat and Human Vascular Smooth Muscle Cells
From the Department of Medicine (R.E.L., S.G., X.-P.X., S.J., Y.K., L.D., W.P.M., W.A.H.); the Division of Endocrinology, Diabetes, and Hypertension (R.E.L., S.G., X.-P.X., Y.K., W.P.M., W.A.H.); the Division of Cardiology (S.J., L.D.); and the Department of Pathology and Laboratory Medicine (M.C.F.), University of California at Los Angeles School of Medicine.
Correspondence to Ronald E. Law, PhD, UCLA, Warren Hall, Second Floor, Suite 24-130, 900 Veteran Ave, Los Angeles, CA 90095.
Background—Peroxisome
proliferator–activated receptor-
(PPAR) is
activated by fatty acids, eicosanoids, and insulin-sensitizing
thiazolidinediones (TZDs). The TZD troglitazone (TRO) inhibits vascular
smooth muscle cell (VSMC) proliferation and migration in vitro and in
postinjury intimal hyperplasia.
Methods and Results—Rat and human VSMCs express mRNA and nuclear
receptors for PPAR1. Three PPAR ligands, the TZDs TRO and
rosiglitazone and the prostanoid
15-deoxy-
12,14-prostaglandin J2 (15d-PGJ2),
all inhibited VSMC proliferation and migration. PPAR is upregulated
in rat neointima at 7 days and 14 days after balloon injury
and is also present in early human atheroma and
precursor lesions.
Conclusions—Pharmacological activation of PPAR expressed in
VSMCs inhibits their proliferation and migration, potentially limiting
restenosis and atherosclerosis. These receptors
are upregulated during vascular injury.
Key Words: atherosclerosis • restenosis • growth substances • migration • thiazolidinediones
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