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Am J Physiol Heart Circ Physiol 287: H866-H871, 2004. First published April 8, 2004; doi:10.1152/ajpheart.00918.2003
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IL-10 inhibits vascular smooth muscle cell activation in vitro and in vivo

Mikael Mazighi,1 Anne Pellé,1 Walter Gonzalez,1 El Mostafa Mtairag,1 Monique Philippe,1 Dominique Hénin,2 Jean-Baptiste Michel,1 and Laurent J. Feldman1,3

1U460 Institut National de la Santé et de la Recherche Médicale, 2Service d'Anatomo-Pathologie, and 3Département de Cardiologie, Centre Hospitalier Universitaire Bichat-Assistance Publique des Hopitaux de Paris, 75018 Paris, France

Submitted 25 September 2003 ; accepted in final form 25 March 2004

The anti-inflammatory cytokine IL-10 inhibits intimal hyperplasia after stent implantation via a powerful inactivation of monocytes. We tested the hypothesis that IL-10 may also inhibit vascular smooth muscle cell (SMC) activation via the inhibition of the NF-{kappa}B/I-{kappa}B system. The IL-10 receptor was detected in rat SMCs in vitro and in vivo. In LPS-stimulated rat SMCs, 1 ng/ml recombinant murine IL-10 (mIL-10) reduced I-{kappa}B{alpha} and I-{kappa}B{beta} degradation, NF-{kappa}B activation, as well as the expression of the NF-{kappa}B-dependent gene IL-6 by 32%, 31%, 75%, and 19%, respectively (P < 0.05 for all). Similar results were obtained in vivo 6 h and 4 days after balloon abrasion of the rat aorta, a model in which intimal hyperplasia results essentially from SMC activation. Moreover, mIL-10 reduced SMC proliferation and migration in vitro (by 60% for both, P < 0.0001), resulting in reduced SMC proliferation and intimal growth 14 days after balloon abrasion of the rat aorta (by 76% and 75%, respectively; P < 0.005). In conclusion, mIL-10 has a direct inhibitory effect on SMCs in vitro and in vivo. This effect is mediated in part by NF-{kappa}B inactivation and may participate in the overall protective effect of IL-10 on postangioplasty restenosis.

nuclear factor-{kappa}B; intimal hyperplasia; cell migration and proliferation; interleukin-6


Address for reprint requests and other correspondence: L. J. Feldman, Département de Cardiologie, Centre Hospitalier Universitaire Bichat-APHP, 46, rue Henri Huchard, 75018 Paris, France (E-mail: laurent.feldman{at}bch.ap-hop-paris.fr).




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