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—Peroxisome  proliferator–activated receptor-γ (PPARγ) is a key player  in glucose metabolism. If PPARγ ligands modulate nitric  oxide (NO) synthesis in the vascular tissue, they may affect the  process of plaque formation and postangioplasty restenosis. We  investigated the effects of PPARγ ligands on NO synthesis in vascular  smooth muscle cells. Incubation of cultures with interleukin-1β (10  ng/mL) for 24 hours caused a significant increase in the  production of nitrite, a stable metabolite of NO, in cultured  rat vascular smooth muscle cells. The PPARγ agonists troglitazone and  15-deoxy-▵12,14 -prostaglandin J2 (15d-PG J2 ) dose-dependently inhibited nitrite  production by interleukin-1β–stimulated vascular smooth  muscle cells. Decreased interleukin-1β–induced nitrite  production by the PPARγ agonists was accompanied by decreased  inducible NO synthase mRNA and protein accumulation. Interleukin-1β  induced nuclear factor-κB activation in vascular smooth muscle cells,  and both troglitazone and 15d-PG J2 markedly suppressed  this nuclear factor-κB activation. PPARγ ligands inhibit NO  synthesis in cytokine-stimulated vascular smooth muscle cells,  suggesting that these agonists may act directly on the vascular smooth  muscle and influence the process of atherosclerosis  and restenosis.

Peroxisome Proliferator–Activated Receptor-γ Ligands Inhibit Nitric Oxide Synthesis in Vascular Smooth Muscle Cells