A novel adipocytokine, omentin, inhibits platelet-derived growth factor-BB-induced vascular smooth muscle cell migration through antioxidative mechanism

作者：Kazama Kyosuke; Okada Muneyoshi; Yamawaki Hideyuki^*

来源：American Journal of Physiology - Heart and Circulatory Physiology, 2014, 306(12): H1714-H1719.

DOI：10.1152/ajpheart.00048.2014

• adipokine
• vascular smooth muscle
• migration
• oxidative stress
• cell signaling

Omentin is a novel adipocytokine expressed in visceral adipose tissue. Secretion and blood concentration of omentin decrease in the obese subjects. We previously demonstrated that omentin is anti-inflammatory in vascular smooth muscle cells (SMCs). While vascular remodeling via migration of SMCs is also important for hypertension development, it remains to be clarified whether omentin affects this process. Here we examined whether omentin controls SMC migration. Omentin (300 ng/ml, 2 h) significantly inhibited platelet-derived growth factor (PDGF)-BB (10 ng/ml, 6 h)-induced migration of rat mesenteric arterial SMCs, as determined by Boyden chamber assay. Omentin (300 ng/ml, 2 h) significantly inhibited PDGF-BB (10 ng/ml, 30 min)-induced phosphorylation of p38 and heat shock protein (HSP) 27. Omentin (300 ng/ml, 2 h) significantly inhibited PDGF-BB (10 ng/ml, 30 min)-induced NADPH oxidase (NOX) activation as determined by lucigenin assay. Omentin (300 ng/ml, 24 h) significantly inhibited fetal bovine serum (5%, 4 days)-induced SMC outgrowth from rat isolated mesenteric artery. In vivo, omentin significantly inhibited carotid intimal hyperplasia in mouse ligation model. In summary, we for the first time demonstrate that omentin prevents PDGF-BB-induced SMC migration by preventing NOX/O-2(-)/p38/HSP27 pathways, which might be at least partly responsible for the preventive effects on neointimal hyperplasia. Our data suggest that omentin may be protective against hypertension development by inhibiting vascular structural remodeling.

• 出版日期2014-6-15