EDIL3 depletion suppress epithelial-mesenchymal transition of lens epithelial cells via transforming growth factor β pathway

作     者：Rui Zhang You-Heng Wei Chun-Yan Zhao Hong-Yuan Song Ni Shen Xiao Cui Xin Gao Zhong-Tian Qi Ming Zhong Wei Shen 

作者机构：Department of Ophthalmology Changhai Hospital Second Military Medical University State Key Laboratory of Genetic Engineering Institute of Genetics School of Life Sciences Fudan University Department of Microbiology Second Military Medical University 

出 版 物：《International Journal of Ophthalmology(English edition)》 (国际眼科杂志（英文版）)

年 卷 期：2018年第11卷第1期

页      面：18-24页

核心收录：

学科分类：1002[医学-临床医学] 100212[医学-眼科学] 10[医学] 

基　　金：Supported by the National Natural Science Foundation of China (No.81700839) Military logistics scientific research project (No.BWS12J030) Natural Science Foundation of Shanghai (No.15ZR1413200) Research Foundation for Youth of Second Military Medical University (No.2016QN13) Research Foundation for Youth of Changhai Hospital (No.CH201712) 

主　　题：discoidin I like domain containing protein 3 transforming growth factor β epithelial mesenchymal transition human lens epithelial cells 

摘      要：AIM： To study the effect of discoidin I-like domaincontaining protein 3（EDIL3） depletion on the proliferation and epithelial-mesenchymal transition（EMT） in human lens epithelial cells（LECs）. METHODS： RNA interference was used to inhibit the expression of EDIL3 in human LECs in vitro. The morphology of cells was observed using an inverted microscope. Cell proliferation was assessed using Ed U kit. Cell migration was investigated using Transwell chamber and EMT of LECs was assessed using confocal microscope and Western blotting. The transforming growth factor β（TGFβ） pathway was investigated using Western blotting. RESULTS： The data showed that silencing EDIL3 expression changed LECs morphology and suppressed LECs proliferation（P〈0.05） and migration（P〈0.01）. Furthermore, the result of Western blotting showed that EDIL3 depletion reduced the expression of α-smooth muscle actin（α-SMA）（P〈0.001） and vimentin（P〈0.01）, while increased the expression of E-cadherin（P〈0.001）. EDIL3 depletion could suppress the phosphorylation of Smad2（P〈0.01） and Smad3（P〈0.01） and the activation of exracellular signal regulated kinase（ERK）（P〈0.05）. CONCLUSION： The findings indicate that EDIL3 might participate in the proliferation and EMT in LECs via TGFβ pathway and may be a potential therapeutic target for the treatment of posterior capsule opacification.