Promotion of autophagy and inhibition of apoptosis by low concentrations of cadmium in vascular endothelial cells

Recent reports, highlighting the relationships of cadmium exposure and vascular diseases, indicated that vascular endothelial cell was the target of cadmium (Cd) toxicity. However, the underlying mechanisms have not been fully elucidated. In this study, we evaluated the internalization of Cd(2+) into human umbilical vein endothelial cells (HUVECs) by a novel Cd(2+)-selective sensor suitable for living cells. Then, we detected apoptosis in the treated cells. Our results showed that Cd(2+) at low concentrations (<10 μmol/l) inhibited apoptosis induced by deprivation of serum and basic fibroblast growth factor (bFGF). To investigate the corresponding molecular mechanisms, we employed acridine orange staining and Western blotting of MAP1 LC3 to detect autophagy, and analyzed the levels of integrin β4, caveolin-1 and activity of PC-PLC. Our results showed that low concentrations of Cd(2+) promoted autophagy and depressed the levels of integrin β4, caveolin-1 and PC-PLC activity. The data suggested that autophagy played a key role in Cd(2+) induced endothelial dysfunction; integrin β4, caveolin-1 and PC-PLC might be the targets of Cd(2+) in vascular endothelial cells.