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Background: The present study focuses on the evaluation of the protective effect on retinal neovascularization exerted by melanocortin receptor 1–5 (MCR 1–5) agonists in a mouse model of proliferative retinopathy induced by intravitreal injection of vascular endothelial growth factor 165 (VEGF165). Methods: Intravitreal injections of the MCR1 agonist BMS-470539 and of the MCR5 agonist PG-901 were performed 7 days before the VEGF165 injection and 1 day after VEGF165 injection. Fluorescein angiography (FAG), immunohistochemical and biochemical analysis were performed at different time points during the follow up. Results: FAG showed a marked vascular tortuosity accompanied by retinal neovascularization in mice receiving VEGF165 intravitreal injection and the absence of neovascularization in mice treated with MCR 1–5 agonists, confirmed by CD34 antigen immunostaining. The biochemical analysis of retinal VEGFR2 gene and protein expression showed that MCR 1–5 agonists significantly reduced VEGFR2 levels, increasing in parallel retinal mir-150 expression. Conclusions: According to these evidences, we propose that intravitreal injections of melanocortin receptor agonists up-regulate mir-150 expression, and this consequently reduces VEGFR2 expression levels with the endpoint being the blockade of VEGF165 induced retinopathy.

Intravitreal Injections of Melanocortin Receptor 1, 5 Agonists Prevents Neovascularization in a VEGF165 Mouse Model of Retinopathy