Atorvastatin increases endothelial progenitor cells in balloon-injured mouse carotid artery.

Abstract

Here we aimed to investigate the effects of atorvastatin on accelerated reendothelialization after carotid balloon injury. A mouse model of carotid arterial injury was established, followed by intragastric administration of atorvastatin at a dose of 0.6 mg·(kg body mass)(-1)·d(-1). Pathological sections of carotid artery stained with hematoxylin and eosin were observed under light microscopy. Expression levels of eNOS mRNA and protein were detected with real-time quantitative PCR and Western blot analysis, respectively. Proliferation and differentiation of endothelial progenitor cells (EPCs) were observed after treatment, in vitro. Reendothelialization appeared on the neovascular surface, while intimal hyperplasia was inhibited after treatment with atorvastatin. Numbers of CD31-positive cells increased after atorvastatin treatment, as did the number of leucocyte antigen positive cells. The expression of cell markers, such as CD34, eNOS, and VEGF-R, were higher in the atorvastatin-treated group of mononuclear cells. EPC numbers increased with the concentration of atorvastatin. The expression of eNOS mRNA was reduced in the mice with carotid artery injury that were treated with normal saline. The expression levels of eNOS protein were increased in atorvastatin treatment group. In conclusion, atorvastatin stimulates EPCs to differentiate into endothelial cells and promotes the repair of carotid arterial injury.