Apoptosis of lens epithelial cells induced by high concentration of glucose is associated with a decrease in caveolin-1 levels.

purposeLens epithelial cell (LEC) apoptosis reduces the formation of posterior capsular opacification (PCO). The involvement of caveolin-1 in the regulation of apoptosis has been previously demonstrated in epithelial cells. In this study, we investigated the relationship between caveolin-1 and apoptosis of LECs under high glucose (HG) concentrations to explore a mechanism in the formation of PCO in diabetic patients.

methodsLECs were treated with high concentrations of glucose with or without epidermal growth factor (EGF) or simvastatin in Dulbecco's Modified Eagle's Medium (DMEM). Induction of apoptosis was measured by flow cytometry, and the expression of caveolin-1 was examined by immunofluorescence microscopy, quantitative real-time reverse transcription polymerase chain reaction (RT-PCR), and immunoblotting.

resultsThe expression of caveolin-1 was decreased, and the rate of apoptosis was increased in LECs treated with increased glucose concentration and treatment duration. When simvastatin or EGF was added to HG-treated LECs, caveolin-1 levels increased and the apoptosis rate of LECs decreased. Furthermore, colocalization of caveolin-1 and phosphatidylserine (PS) on the cell surfaces of apoptotic LECs was observed by immunofluorescence microscopy.

conclusionsWe observed that in HG-treated LECs, caveolin-1 expression decreased and apoptosis increased and that simvastatin or EGF promoted the proliferation of HG-treated LECs. Although the mechanisms for the formation of PCO after cataract surgery in diabetic patients are complex, our results suggest that a high concentration of glucose is not a direct cause. The observation that simvastatin inhibited the apoptosis of HG-treated LECs in its therapeutic concentration suggests that daily dosage of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor used by diabetic patients may increase PCO formation.