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Am J Physiol Heart Circ Physiol (April 8, 2004). doi:10.1152/ajpheart.00918.2003
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Submitted on September 25, 2003
Accepted on March 25, 2004

Interleukin-10 Inhibits Vascular Smooth Muscle Cell Activation In Vitro and In Vivo

Mikael Mazighi1, Anne Pelle1, Walter Gonzalez1, El Mostafa Mtaraig1, Monique Philippe1, Dominique Henin1, Jean-Baptiste Michel1, and Laurent J. Feldman1*

1 Service d'Anatomo-Pathologie and Departement de Cardiologie, CHU Bichat-APHP, U 460 INSERM, Paris, France

* To whom correspondence should be addressed. E-mail: laurent.feldman{at}bch.ap-hop-paris.fr.

The anti-inflammatory cytokine interleukin-10 (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 6h 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, at least in part, by NF-{kappa}B inactivation and may participate in the overall protective effect of IL-10 on post-angioplasty restenosis.




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