增殖性玻璃体视网膜病变
上皮-间质转换
小窝蛋白1
基因敲除
发病机制
下调和上调
癌症研究
细胞迁移
污渍
细胞生物学
病理
免疫组织化学
间充质干细胞
生物
细胞
细胞培养
视网膜
医学
视网膜脱离
眼科
生物化学
遗传学
基因
作者
Yosuke Nagasaka,Hiroki Kaneko,Fuxiang Ye,Shu Kachi,Tetsu Asami,Seiichi Kato,Kei Takayama,Shiang-Jyi Hwang,Keiko Kataoka,Hideyuki Shimizu,Takeshi Iwase,Yasuhito Funahashi,Akiko Higuchi,Takeshi Senga,Hiroko Terasaki
标识
DOI:10.1167/iovs.16-20513
摘要
Purpose: Proliferative vitreoretinopathy (PVR) is one of the most severe ocular diseases. Fibrotic changes in retinal cells are considered to be involved in the pathogenesis of PVR. Epithelial-mesenchymal transition (EMT) of RPE cells is one of the main concepts in the pathogenesis of fibrovascular membranes (FVMs) in PVR. In this study, we examined the expression of Caveolin-1 in human FVMs from patients with PVR. We also examined the role of Caveolin-1 in the pathogenesis of PVR. Methods: Western blotting, real-time PCR, and immunohistochemistry were performed with human FVMs and mouse eyes with PVR. Cell migration assays were performed to evaluate the involvement of Caveolin-1 in EMT using primary human and mouse RPE cells. Results: Caveolin-1 was expressed in human FVMs and upregulated in the mouse eyes with PVR. The alpha-smooth muscle actin (αSMA) expression and migration ability were increased in RPE cells with knockout or knockdown of Caveolin-1, whereas zonula occludens-1 (ZO-1) immunohistochemistry showed reduced morphology and expression of ZO-1. In addition, migration assays showed that Caveolin-1 reduction increased RPE cell migration abilities. Conclusions: These results indicated that Caveolin-1 in RPE cells prevents PVR by blocking EMT.
科研通智能强力驱动
Strongly Powered by AbleSci AI