Regulation and Mechanism of Chloride Channels in Proliferative Vitreoretinopathy

Abstract

Abstract Background This study aimed to investigate the regulation of chloride channels in proliferative vitreoretinopathy (PVR) both in vitro and in vivo using a rabbit model and to explore the underlying mechanism. Methods The chloride channel was regulated by the chloride channel inhibitor NPPB and the chloride channel activator lubiprostone. RPE cell proliferation and migration were assessed using CCK-8, cell scratch, and Transwell assays. Collagen I, Collagen III, and Fibronectin protein levels were detected by Western blotting. In the in vivo study, NPPB or lubiprostone was injected intravitreally to induce the PVR model. PVR severity was evaluated based on histological Western blotting, which detected Collagen I, Collagen III, and Fibronectin protein levels. Results Lubiprostone promoted TGF-β1-induced ARPE 19 cell growth and invasion, thereby facilitating PVR formation, while NPPB had the opposite effect, inhibiting PVR formation. Consistent results were also observed in in vivo models. Conclusions Reducing the opening of chloride channels within RPE cells using drugs can suppress PVR formation, which is sufficient to explain retinal degeneration. Chloride channels may have a crucial impact on RPE cell proliferation and migration. The therapeutic strategy of blocking chloride channels may be beneficial for PVR.