TGF-β2诱导晶状体上皮细胞凋亡的机制

Objective: To investigate the effects of transforming growth factor-beta 2 (TGF-β2) on the apoptosis of human lens epithelial cells (HLECs) in posterior capsular opacification (PCO). Methods: Different concentration (0, 0.1, 1, and 10 μg/L) of TGF-β2 was added into HLECs to induce cell apoptosis and Western blot was applied to analyze the expression levels of endogenous mitochondrial pathway-dependent apoptosis-associated proteins. Flow cytometry was used to measure the cell apoptosis and cell cycle arrest induced by 5μg/L of TGF-β2. Results: TGF-β2 was sufficient to significantly increase the expression of apoptosis-associated proteins such as Caspase3 (P<0.001) and expression imbalance of Bcl-2/Bax (P<0.001) in the concentration-dependent manner, indicating the activation of endogenous mitochondrial apoptosis pathway. Stimulation of 5 μg/L of TGF-β2 was enough to induce cell apoptosis (P<0.05). After induction for 36 h, obvious G1/S cell cycle arrest was observed. Conclusion: TGF-β2 was involved in the mitochondrial apoptosis pathway and PCO. Our findings might provide new insights into the pathogenesis and new drug exploitation for PCO.