Journal
CIRCULATION
Volume 101, Issue 11, Pages 1311-1318Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/01.CIR.101.11.1311
Keywords
atherosclerosis; restenosis; growth substances; migration; thiazolidinediones
Funding
- NHLBI NIH HHS [HL58328-03] Funding Source: Medline
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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.
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