Antagonist of nucleolin, N6L, inhibits neovascularization in mouse models of retinopathies.

摘要: Retinal vascular diseases (RVD) have been identified as a major cause of blindness worldwide. These pathologies, including the wet form age-related macular degeneration, retinopathy prematurity, and diabetic are currently treated by intravitreal delivery anti-vascular endothelial growth factor (VEGF) agents. However, repeated injections can lead to ocular complications resistance these treatments. Thus, there is need find new targeted therapies. Nucleolin regulates cell (EC) activation angiogenesis. In previous studies, we designed pseudopeptide, N6L, that binds nucleolin blocks tumor this study, effect N6L was investigated in two experimental models retinopathies oxygen-induced (OIR) choroidal neovascularization (CNV). We found mouse OIR, intraperitoneal injection delivered activated ECs induced 50% reduction pathological neovascularization. The anti-angiogenic has tested CNV model which systemic 33% This comparable those obtained with VEGF-trap, standard care drug for RVD. Interestingly, preventive curative treatments, neoangiogenesis inhibited 59%. Our results potential interest development therapies targeting other molecules than VEGF