First Author | Nagasaka Y | Year | 2017 |
Journal | Invest Ophthalmol Vis Sci | Volume | 58 |
Issue | 1 | Pages | 221-229 |
PubMed ID | 28114583 | Mgi Jnum | J:254647 |
Mgi Id | MGI:6112550 | Doi | 10.1167/iovs.16-20513 |
Citation | Nagasaka Y, et al. (2017) Role of Caveolin-1 for Blocking the Epithelial-Mesenchymal Transition in Proliferative Vitreoretinopathy. Invest Ophthalmol Vis Sci 58(1):221-229 |
abstractText | 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 (alphaSMA) 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. |