Expression and Function of PPARg in Rat and Human Vascular Smooth Muscle Cells
نویسندگان
چکیده
Background—Peroxisome proliferator–activated receptor-g (PPARg) 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 PPARg1. Three PPARg ligands, the TZDs TRO and rosiglitazone and the prostanoid 15-deoxy-D-prostaglandin J2 (15d-PGJ2), all inhibited VSMC proliferation and migration. PPARg 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 PPARg expressed in VSMCs inhibits their proliferation and migration, potentially limiting restenosis and atherosclerosis. These receptors are upregulated during vascular injury. (Circulation. 2000;101:1311-1318.)
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