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Research Article Free access | 10.1172/JCI119038

Rapamycin inhibits vascular smooth muscle cell migration.

M Poon, S O Marx, R Gallo, J J Badimon, M B Taubman, and A R Marks

Cardiovascular Institute, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA.

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Cardiovascular Institute, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA.

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Cardiovascular Institute, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA.

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Cardiovascular Institute, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA.

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Cardiovascular Institute, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA.

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Cardiovascular Institute, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA.

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Published November 15, 1996 - More info

Published in Volume 98, Issue 10 on November 15, 1996
J Clin Invest. 1996;98(10):2277–2283. https://doi.org/10.1172/JCI119038.
© 1996 The American Society for Clinical Investigation
Published November 15, 1996 - Version history
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Abstract

Abnormal vascular smooth muscle cell (SMC) proliferation and migration contribute to the development of restenosis after percutaneous transluminal coronary angioplasty and accelerated arteriopathy after cardiac transplantation. Previously, we reported that the macrolide antibiotic rapamycin, but not the related compound FK506, inhibits both human and rat aortic SMC proliferation in vitro by inhibiting cell cycle-dependent kinases and delaying phosphorylation of retinoblastoma protein (Marx, S.O., T. Jayaraman, L.O. Go, and A.R. Marks. 1995. Circ. Res. 362:801). In the present study the effects of rapamycin on SMC migration were assayed in vitro using a modified Boyden chamber and in vivo using a porcine aortic SMC explant model. Pretreatment with rapamycin (2 ng/ml) for 48 h inhibited PDGF-induced migration (PDGF BB homodimer; 20 ng/ml) in cultured rat and human SMC (n = 10; P < 0.0001), whereas FK506 had no significant effect on migration. Rapamycin administered orally (1 mg/kg per d for 7 d) significantly inhibited porcine aortic SMC migration compared with control (n = 15; P < 0.0001). Thus, in addition to being a potent immunosuppressant and antiproliferative, rapamycin also inhibits SMC migration.

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