Expression and function of PPARγ in rat and human vascular smooth muscle cells

被引：408

作者：

Law, RE

Goetze, S

Xi, XP

Jackson, S

Kawano, Y

Demer, L

Fishbein, MC

Meehan, WP

Hsueh, WA

机构：

[1] Univ Calif Los Angeles, Sch Med, Dept Med, Los Angeles, CA 90095 USA

[2] Univ Calif Los Angeles, Sch Med, Div Endocrinol Diabet & Hypertens, Los Angeles, CA 90095 USA

[3] Univ Calif Los Angeles, Sch Med, Div Cardiol, Los Angeles, CA 90095 USA

[4] Univ Calif Los Angeles, Sch Med, Dept Pathol & Lab Med, Los Angeles, CA 90095 USA

来源：

CIRCULATION | 2000年 / 101卷 / 11期

关键词：

atherosclerosis; restenosis; growth substances; migration; thiazolidinediones;

D O I：

10.1161/01.CIR.101.11.1311

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Background-Peroxisome proliferator-activated receptor-gamma (PPAR gamma) 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 PPAR gamma 1. Three PPAR gamma ligands, the TZDs TRO and rosiglitazone and the prostanoid 15-deoxy-Delta(12,14)-prostaglandin J2 (15d-PGJ2), all inhibited VSMC proliferation and migration. PPAR gamma 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 gamma expressed in VSMCs inhibits their proliferation and migration, potentially limiting restenosis and atherosclerosis. These receptors are upregulated during vascular injury.

引用

页码：1311 / 1318

页数：8

共 33 条

[1] Thiazolidinediones produce a conformational change in peroxisomal proliferator-activated receptor-gamma: Binding and activation correlate with antidiabetic actions in db/db mice [J].