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

Autor: El Mostafa Mtairag, Walter Gonzalez, Laurent J. Feldman, Mikael Mazighi, Jean-Baptiste Michel, Monique Philippe, Anne Pellé, Dominique Hénin
Rok vydání: 2004
Předmět:
Zdroj: American Journal of Physiology-Heart and Circulatory Physiology. 287:H866-H871
ISSN: 1522-1539
0363-6135
DOI: 10.1152/ajpheart.00918.2003
Popis: 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-kappaB/I-kappaB 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-kappaBalpha and I-kappaBbeta degradation, NF-kappaB activation, as well as the expression of the NF-kappaB-dependent gene IL-6 by 32%, 31%, 75%, and 19%, respectively (P0.05 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, P0.0001), resulting in reduced SMC proliferation and intimal growth 14 days after balloon abrasion of the rat aorta (by 76% and 75%, respectively; P0.005). In conclusion, mIL-10 has a direct inhibitory effect on SMCs in vitro and in vivo. This effect is mediated in part by NF-kappaB inactivation and may participate in the overall protective effect of IL-10 on postangioplasty restenosis.
Databáze: OpenAIRE