Role of cyclic adenosine monophosphate-response element binding protein in hypertonic-induced cell injury in human lens epithelial cells

Abstract Purpose: Diabetic cataracts is one of the complication of diabetes mellitus which contributes to the opacification of the lens and blindness by hurting lens epithelial cells (LECs). The hypertonic environment due to the high blood glucose level is a most important reason of LECs injury in diabetes mellitus. However, the mechanism of LEC self-regulation under a hypertonic condition is still not fully understood. This study aims to investigated the function of cyclic adenosine monophosphate-response element binding protein (CREB) and its related mitogen-activated protein kinase (MAPK) pathways, mitochondria-related proteins in regulating of cell viability process of LECs, under hypertonic conditions.Method: We exposed lens epithelial cells to hypertonic conditions to detect the activation of CREB and MAPK pathways and the changes of mitochondrial related proteins in cells,to verify the effect of CREB on cell injury under hypertonic conditionsResults: We found that CREB can attenuate LEC cell viability under hypertonic conditions. Additionally, we found that the activation of proteins in MAPK and apoptosis-related pathways may be responsible for the cellular signaling mechanism of CREB-mediated protection.Conclusion: CREB protects LECs against the hypertonic solution-induced damage by suppressing p53-mediated mitochondria-dependent apoptotic signaling. In addition, activation of extracellular signal-regulated protein kinase 1/2, p38 MAPKs, and B-cell leukemia/lymphoma 2 expression may underlie CREB-mediated protection.