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

Abstract

Our results indicate that eNOS deficiency exacerbates CAL-induced expression of SDF-1alpha and its receptor CXCR4. This is correlated with an increase in Sca-1(+) cells in peripheral blood and adventitia, which may contribute to vascular remodeling and SMC-rich neointimal lesion formation. This suggests that constitutive eNOS inhibits SDF-1alpha expression and provides an important vasculoprotective mechanism for intact endothelium to limit SMC proliferation and recruitment in response to vascular injury.