(Background) Omentin, a novel adipocytokine, is mainly expressed in the visceral rather than subcutaneous adipose tissue. Secretion and plasma 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 proliferation, migration and apoptosis of SMCs is also important for hypertension development, it remains to be clarified whether omentin affects those processes.
(Methods and Results) Cultured rat mesenteric arterial SMCs were stimulated with platelet-derived growth factor (PDGF)-BB (10 ng/ml) in the absence or presence of omentin (300 ng/ml). Omentin pretreatment (2 h) inhibited PDGF (6 h)-induced SMCs migration (30 % inhibition, n=11, P<0.05) as determined by Boyden camber assay. Omentin pretreatment (2 h) inhibited NADPH oxidase -derived O2- generation as determined by dihydroethidium staining and lucigenin assay (30 % inhibition, n=5, P<0.05) as well as phosphorylation of p38 (20 % inhibition, n=19-23, P<0.01) and heat shock protein (HSP) 27 (20 % inhibition, n=14-17, P<0.01) as determined by Western blotting. Omentin pretreatment (2 h) inhibited PDGF (6 h)-induced lamellipodia formation as determined by rhodamine-phalloidin staining. In ex vivo, omentin pretreatment (6 h) also inhibited fetal bovine serum (FBS) (10%)-induced SMCs out-growth from rat isolated mesenteric artery.
(Conclusion) We for the first time demonstrate that omentin prevented SMCs migration by preventing the activation of ROS-dependent p38/HSP27 signals. It is suggested that omentin is anti-hypertensive ‘good adipocytokine’.