Abstract
Neovascular age related macular degeneration (nAMD) leads to severe vision loss worldwide and is characterized by the formation of choroidal neovascularization (CNV) and fibrosis. In the current study, we aimed to investigate the effect of blockade for platelet derived growth factor receptor-β (PDGFR-β) on the formation of choroidal neovascularization and fibrosis in the laser-induced CNV model in mice. Firstly, the presence of PDGFR-β in CNV lesions were confirmed. Intravitreal injection of PDGFR-β neutralizing antibody significantly reduced the size of CNV and subretinal fibrosis. Additionally, subretinal hyperreflective material (SHRM), a landmark feature on OCT as a risk factor for subretinal fibrosis formation in nAMD patients was also suppressed by PDGFR-β blockade. Furthermore, pericytes were abundantly recruited to the CNV lesions during CNV formation, however, blockade of PDGFR-β significantly reduced pericyte recruitment. In addition, PDGF-BB stimulation increased the migration of the rat retinal pericyte cell line, R-rPCT1, which was abrogated by the neutralization of PDGFR-β. These results indicate that blockade of PDGFR-β attenuates laser-induced CNV and fibrosis through the inhibition of pericyte migration.
Highlights
Age-related macular degeneration (AMD) is the leading cause of irreversible blindness worldwide in developed countries [1]
We investigated whether blockade of platelet derived growth factor receptor-β (PDGFR-β) signaling suppresses the formation of choroidal neovascularization (CNV) and subretinal fibrosis in laser-induced CNV mice
To determine whether PDGFR-β blockade suppresses CNV formation, mice were treated with either APB5, a PDGFR-β neutralizing antibody, or isotype matched IgG immediately after laser injury
Summary
Age-related macular degeneration (AMD) is the leading cause of irreversible blindness worldwide in developed countries [1]. The neovascular type of AMD (nAMD) leads to severe vision loss and is characterized by the formation of choroidal neovascularization (CNV), which extends from the choroid into the subretinal space and disrupts Bruch’s membrane and the retinal pigment epithelium (RPE). The formation of CNV is subsequently followed by the development of subretinal fibrosis, resulting in permanent photoreceptor damage and severe vision loss [2,3,4,5]. A large number of patients receiving anti-VEGF treatment suffered from poor visual prognosis due to subretinal fibrosis [2]. Alternative therapeutic approaches, which potentially attenuate both CNV and subretinal fibrosis development, would fulfill an unmet medical demand in the treatment of nAMD
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
