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Research Article Free access | 10.1172/JCI118991

Troglitazone inhibits vascular smooth muscle cell growth and intimal hyperplasia.

R E Law, W P Meehan, X P Xi, K Graf, D A Wuthrich, W Coats, D Faxon, and W A Hsueh

University of Southern California School of Medicine, Department of Medicine, Los Angeles 90033, USA.

Find articles by Law, R. in: JCI | PubMed | Google Scholar

University of Southern California School of Medicine, Department of Medicine, Los Angeles 90033, USA.

Find articles by Meehan, W. in: JCI | PubMed | Google Scholar

University of Southern California School of Medicine, Department of Medicine, Los Angeles 90033, USA.

Find articles by Xi, X. in: JCI | PubMed | Google Scholar

University of Southern California School of Medicine, Department of Medicine, Los Angeles 90033, USA.

Find articles by Graf, K. in: JCI | PubMed | Google Scholar

University of Southern California School of Medicine, Department of Medicine, Los Angeles 90033, USA.

Find articles by Wuthrich, D. in: JCI | PubMed | Google Scholar

University of Southern California School of Medicine, Department of Medicine, Los Angeles 90033, USA.

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University of Southern California School of Medicine, Department of Medicine, Los Angeles 90033, USA.

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University of Southern California School of Medicine, Department of Medicine, Los Angeles 90033, USA.

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Published October 15, 1996 - More info

Published in Volume 98, Issue 8 on October 15, 1996
J Clin Invest. 1996;98(8):1897–1905. https://doi.org/10.1172/JCI118991.
© 1996 The American Society for Clinical Investigation
Published October 15, 1996 - Version history
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Abstract

Vascular smooth muscle cell (VSMC) proliferation and migration are responses to arterial injury that are highly important to the processes of restenosis and atherosclerosis. In the arterial balloon injury model in the rat, platelet-derived growth factor (PDGF) and basic fibroblast growth factor (bFGF) are induced in the vessel wall and regulate these VSMC activities. Novel insulin sensitizing agents, thiazolidinediones, have been demonstrated to inhibit insulin and epidermal growth factor-induced growth of VSMCs. We hypothesized that these agents might also inhibit the effect of PDGF and bFGF on cultured VSMCs and intimal hyperplasia in vivo. Troglitazone (1 microM), a member of the thiazolidinedione class, produced a near complete inhibition of both bFGF-induced DNA synthesis as measured by bromodeoxyuridine incorporation (6.5+/-3.9 vs. 17.6+/-4.3% cells labeled, P < 0.05) and c-fos induction. This effect was associated with an inhibition (by 73+/-4%, P < 0.01) by troglitazone of the transactivation of the serum response element, which regulates c-fos expression. Inhibition of c-fos induction by troglitazone appeared to occur via a blockade of the MAP kinase pathway at a point downstream of MAP kinase activation by MAP kinase kinase. At this dose, troglitazone also inhibited PDGF-BB-directed migration of VSMC (by 70+/-6%, P < 0.01). These in vitro effects were operative in vivo. Quantitative image analysis revealed that troglitazone-treated rats had 62% (P < 0.001) less neointima/media area ratio 14 d after balloon injury of the aorta compared with injured rats that received no troglitazone. These results suggest troglitazone is a potent inhibitor of VSMC proliferation and migration and, thus, may be a useful agent to prevent restenosis and possibly atherosclerosis.

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