Cardioprotective role of vitamin D receptor in circulating endothelial cells of ApoE-deficient mice.

Atherosclerosis is the key course of coronary heart disease. In this study, we investigated the effect of vitamin D receptor on serum 1,25-(OH)2D levels, lipid profiles, nitric oxide expression, apoptosis-related gene Bcl-2, fas protein levels, in ApoE-deficient mice. The proliferation activity of VDR-RNAi transfected endothelial cells was decreased, the ability of apoptosis was increased, nitric oxide concentration was decreased and eNOS protein level was significantly reduced. VDR-RNAi induced lipid metabolism abnormality, reduced eNOS and ApoE levels, promoted lipid peroxidation, damaged the endothelial function and accelerated the process of atheroscleros. Together, our data presented a novel role for VDR in the pathogenesis process of atheroscleros by up regulating eNOS protein expression which could lay a solid foundation of VDR-specific activator treatment for coronary artery disease.