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Endothelial NO deficiency (endothelial NO synthase [eNOS]-knockout [KO]) enhanced smooth muscle cell (SMC)-rich neointimal lesion formation in a mouse model of carotid artery ligation (CAL). Recent evidence indicated that stromal cell-derived factor-1alpha (SDF-1alpha)-mediated recruitment of circulating SMC progenitor cells substantially contributed to the SMC-rich neointimal hyperplasia induced by vascular injury. The goal of this study was to investigate the effects of eNOS deficiency on the expression of SDF-1alpha and mobilization of circulating SMC progenitor cells in CAL model.

arteriosclerosis, thrombosis, and vascular biology

Endothelial NO Synthase Deficiency Promotes Smooth Muscle Progenitor Cells in Association With Upregulation of Stromal Cell-Derived Factor-1α in a Mouse Model of Carotid Artery Ligation