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High glucose concentration induces retinal endothelial cell apoptosis by activating p53 signaling pathway.

Diabetic retinopathy (DR) is a retinal disease in patients with diabetes caused by metabolic disorders of glucose, and often leads to irreversible blindness if not treated properly. Dysfunction of retinal endothelial cells (RECs) contributes to the pathogenesis of DR. In the present study we investigated the apoptotic effect of high glucose concentration. High glucose was used to induce cell injury. LDH assay kit was used to detect the leakage of LDH. Western blot was used to detect the expression of bax, cleaved-caspase-3, bcl-2 and p53 proteins. The transmission electron microscope was used to observe apoptotic morphological changes. In the present study, we found that the LDH leakage ratio was significant increased after exposing to 30 mmol/L glucose for 12 h, and both showed a concentration-department manner and time dependent fashion. Next, obvious apoptotic morphological changes were observed after treating the cells with glucose at 30 mmol/L. Further research indicated that the protein levels of p53, pro-apoptotic cleaved-caspase-3, and bax were significantly upregulated, and the level of bcl-2 was decreased after treating with glucose at 30 mmol/L. The protein levels of bax and cl-caspase-3 were significantly decreased and the expression of bcl-2 was increased after pretreated with p53 specific inhibitor pifithrin-α. In conclusion, high glucose concentration induces apoptosis in retinal endothelial cells by activating p53 signaling pathway.