The Mechanism Of TGF-β₂ Regulates Epithelial-mesenchymal Transition In Posterior Capsular Opacification Via Its Autophagic Function

Purpose:This study aims to explore the mechanism of TGF-β2 regulates epithelialmesenchymal transition in posterior capsular opacification(PCO)via its autophagic functions,so as to provide new information for the treatment of PCO.Methods:We used PCR,western blotting,immunofluorescence to detect the effect of different concentrations of TGF-β2 on the expression level of autophagy-related proteins,like LC3,p62,Atg5 and Beclin-1.The formation of autophagosome was observed by transmission electron microscopy to explore the impact of TGF-β2 on autophagy and autophagy flow in human lens epithelial cells.Then,the specific effect of TGF-β2 on autophagy and EMT were detected with or without the TGF-β2 receptor inhibitor SB431542.At last,under the conditions of using rapamycin to induce autophagy or 3-MA to inhibit autophagy,the expression of EMT-related markers were measured.Results:The results shown that TGF-β2 induced autophagy and autophagy flow specifically in a dose?dependent manner in human lens epithelial cells,that is,the expression of autophagy-related protein LC3、Atg5、Beclin-1 increased and the P62 decreased.At the same time,compared with the control group,the number of autophagosome in TGF-β2group was significantly increased under transmission electron microscope.Induction of autophagy promotes EMT progress,and inhibition of autophagy prevents the EMT progress,suggesting that TGF-β2-autophagy has regulatory effect on EMT.Conclusion:In this study,we first found that TGF-β2 induced autophagy in human lens epithelial cells.And autophagy has a regulaed effect on EMT,which is the main cause of posterior cataract.Therefore,TGF-β2-autophagy,as a potential mechanism,provided a research basis for a deeper understanding of the pathogenesis and a new clue for the prevention and drug therapy of PCO.