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 Ca2+. 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/cm2 irradiation for 15 min and then cultured for 24 h. The changes in intracellular Ca2+ were detected by colorimetry, and the protein expression levels of Bad, Bcl‑2 and caspase‑12 were measured by western blot analysis. The intracellular Ca2+ concentration of control HLECs increased significantly following UVB irradiation, whereas in Calb1‑overexpressing cells, the Ca2+ levels remained steady. In the control cells, the expression of Bad and caspase‑12 was upregulated, and that of Bcl‑2 was downregulated. 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 Ca2+. On the whole, the findings of the present study indicate that UVB exposure can lead to an imbalance in the intracellular Ca2+ 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 Ca2+.