Protective effects of calbindin-D28K on the UVB radiation-induced apoptosis of human lens epithelial cells

Calbindin-D28K (Calb1) may protect human lens epithelial cells (HLECs) from apoptosis, which is a process resulting in individual cell death. The protective effects of Calb1 may be attributed to buffering high concentrations of Ca(2+). The present study investigated the mechanisms through which Calb1 protects SRA01/04 cells (a human lens epithelial cell line) against apoptosis induced by ultraviolet B (UVB) exposure. Cells transfected with a lentivirus overexpressing Calb1 and control cells were treated with 40 µW/cm(2) irradiation for 15 min and then cultured for 24 h. The changes in intracellular Ca(2+) were detected by colorimetry, and the protein expression levels of Bad, Bcl-2 and caspase-12 were measured by western blot analysis. The intracellular Ca(2+) concentration of control HLECs increased significantly following UVB irradiation, whereas in Calb1-overexpressing cells, the Ca(2+) levels remained steady. In the control cells, the expression of Bad and caspase-12 was upregulated, and that of Bcl-2 was down-regulated. Notably, during UVB radiation-induced apoptosis, the overexpression of Calb1 inhibited cell death, resulting in the decreased expression of Bad and caspase-12, and in the upregulated expression of Bcl-2. These results suggested that Calb1 inhibited the upregulation of genes involved in apoptosis. The siRNA-mediated knockdown of Calb1 resulted in increased rates of UVB radiation-induced apoptosis, the increased expression of Bad and caspase-12, and the decreased expression of Bcl-2, further demonstrating that Calb1 may mediate UVB radiation-mediated apoptosis by regulating Ca(2+). On the whole, the findings of the present study indicate that UVB exposure can lead to an imbalance in the intracellular Ca(2+) homeostasis in HLECs and that Calb1 protein exerts a negative effect on the expression of pro-apoptotic genes in HLECs. Calb1 may thus inhibit the UVB radiation-induced apoptosis of HLECs by regulating Ca(2+).