视网膜色素上皮细胞（RPE）发生上皮-间充质细胞转换（EMT）是增生性玻璃体视网膜病变（PVR）启动和发展的关键。然而，近年认为RPE细胞发生EMT或PVR是一个被活化的结果，类似于癌细胞从原位转移，首先需要细胞间失去接触；细胞黏着异常是细胞脱落移行的关键元素。前期研究证实，RPE细胞发生EMT前，细胞间黏着蛋白Cadherins发生表达转换（E钙粘素下降和N钙粘素上升），导致黏着连接复合体和相邻细胞间的缝隙连接结构消失，联动Integrin β1表达改变。但是Cadherins表达转换的分子机制尚不清楚。本项目将应用蛋白芯片、生物信息学、细胞分子生物学、电镜和动物实验等方法调查PVR环境下Cadherins蛋白的表达变化及其相关连接蛋白互相作用的机制，证明Cadherins蛋白异常是导致RPE细胞间、与Bruch's膜失去黏着的重要原因。为临床探索PVR治疗新思路奠定基础。

The epithelial-mesenchymal transition (EMT) occured in retinal pigment epithelial cells is thought to play a pivotal role in the pathogenesis of proliferative vitreoretinopathy (PVR). Recent studies suggested that EMT or PVR caused by the activation of RPE cells, similar to the carcinoma metastasis, requires the initially loss of intercellular contacts. Dysregulated cell-cell adhesion is a key factor of cellular falling apart and migration. Our previous studies found that E-cadherin expression switched to N-cadherin in TGF-β1 treated RPE cells, which resulted in the dissociation of adherent junction complex and the loss of intercellular gap junction structure, thereby affecting intergrin β1 expression. However, the mechanisms underlying cadherin switch remain unclear. Our present study is conducted to prove the crucial role of cadherins in the disruption of adhesion between RPE cells and RPE-Bruch's membrane under PVR circumstance. Antibody arrays, bioinformatics analysis, electron microscopy and cell molecular biology technology will be applied to conduct a full investigation and validation. Completion of this project may provide new therapeutic strategies for PVR.