E-cadherin to N-cadherin switching in the TGF-β1 mediated retinal pigment epithelial to mesenchymal transition

被引：15
|
作者：
Wei, Jiayi [1 ]
Wu, Liangjing [1 ]
Yang, Shuai [1 ]
Zhang, Conghui [1 ]
Feng, Le [1 ]
Wang, Minli [1 ]
Li, Hui [1 ]
Wang, Fang [1 ]
机构：
[1] Tongji Univ, Sch Med, Shanghai Peoples Hosp 10, Dept Ophthalmol, 301 Middle Yanchang Rd, Shanghai 200072, Peoples R China
来源：
EXPERIMENTAL EYE RESEARCH | 2022年 / 220卷
基金：
中国国家自然科学基金;
关键词：
E-cadherin; N-cadherin; Retinal pigment epithelium; Epithelial-mesenchymal transition; Proliferative vitreoretinopathy; PROLIFERATIVE VITREORETINOPATHY; BREAST-CANCER; PHENOTYPE; JUNCTIONS; RPE;
D O I：
10.1016/j.exer.2022.109085
中图分类号：
R77 [眼科学];
学科分类号：
100212 ;
摘要：
A serious form of ocular fibrotic disease is proliferative vitreoretinopathy (PVR) that can ultimately lead to blindness. While the pathogenesis of PVR is known to be closely tied to retinal pigment epithelial (RPE) cell epithelial-mesenchymal transition (EMT) characterized by E-cadherin downregulation and N-cadherin upregulation. Herein, we developed a model of transforming growth factor-beta 1 (TGF-beta 1)-induced EMT using human RPE (hRPE) cells as a tool for exploring the mechanistic basis for E-cadherin to N-cadherin switching. This analysis revealed that the loss of E-cadherin led to the separation of beta-catenin from the catenin-cadherin complex whereupon it underwent nuclear entry to activate zinc finger E-box binding homeobox 1 (ZEB1), in turn promoting N-cadherin upregulation in this biological context. E-cadherin overexpression was sufficient to inhibit this EMT process and proliferation in RPE cells, further constraining their TGF-beta 1-induced apoptosis.
引用
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页数：9
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