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IL-10 inhibits vascular smooth muscle cell activation in vitro and in vivo

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-B/I-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-B and I-B degradation, NF-B activation, as well as the expression of the NF-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-B inactivation and may participate in the overall protective effect of IL-10 on postangioplasty restenosis.

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

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