Gaining insight on mitigation of rubeosis iridis by UPARANT in a mouse model associated with proliferative retinopathy.

摘要: Proliferative retinopathies (PR) lead to an increase in neovascularization and inflammation factors, at times culminating pathologic rubeosis iridis (RI). In mice, uveal puncture combined with injection of hypoxia-conditioned media mimics RI associated proliferative retinopathies. Here, we investigated the effects urokinase plasminogen activator receptor (uPAR) antagonist-UPARANT-on angiogenic inflammatory processes that are dysregulated this model. addition, UPARANT were compared those anti-vascular endothelial growth factor (VEGF) therapies. Administration promptly decreased iris vasculature, while anti-VEGF slower less pronounced. Immunoblot qPCR analysis suggested acts predominantly by reducing upregulated extracellular matrix degradation responses. appears be more effective comparison treatment PR murine model, modulating multiple uPAR-associated signaling pathways. Furthermore, effectiveness was maintained when systemically administered, which could open novel improved therapies for ocular diseases, particularly PR. KEY MESSAGES: • Further evidence normalizing pathological neovascularization. Both systemic local administration reduce a model mouse models retinopathy, displays stronger regimen.