Activation of vitamin D receptor promotes VEGF and CuZn-SOD expression in endothelial cells.

ABSTRACT: Endothelial dysfunction associated with vitamin D deficiency has been linked to many chronic vascular diseases. Vitamin D elicits its bioactive actions by binding to its receptor, vitamin D receptor (VDR), on target cells and organs. In the present study, we investigated the role of VDR in response to 1,25(OH)₂D₃ stimulation and oxidative stress challenge in endothelial cells. We found that 1,25(OH)₂D₃ not only induced a dose- and time-dependent increase in VDR expression, but also induced up-regulation of vascular endothelial growth factor (VEGF) and its receptors (Flt-1 and KDR), as well as antioxidant CuZn-superoxide dismutase (CuZn-SOD) expression in endothelial cells. We demonstrated that inhibition of VDR by VDR siRNA blocked 1,25(OH)₂D₃ induced increased VEGF and KDR expression and

SUBMITTER: Zhong W 

PROVIDER: S-EPMC3915503 | biostudies-literature | 2014 Mar

REPOSITORIES: biostudies-literature