Activated Protein C Induces Stabilization Of The Outer Retinal Barrier And Inhibits Laser Induced Choroidal Neovascularization In A Murine Model

Introduction: Age-related macular degeneration (AMD) is considered one of the main causes of severe vision loss in older adults. Wet AMD is characterized by choroidal neovascular membrane developed under or into the sensory retina, breaking the outer blood-retina barrier (oBRB) and causing leakage and bleeding. Protein C (PC) is a plasma serine protease zymogen whose active form, activated protein C (APC), exerts diverse homeostatic cell signaling pathways apart from its anticoagulant activity. APC activities are mediated mainly through endothelial PC receptor (EPCR) and protease activated receptor (PAR)-1. APC was recently shown to act as a novel ligand for Tie2, a tyrosine kinase receptor playing an important role in angiogenesis. Thus, APC may modulate pathological angiogenesis in relevant ocular conditions, such as choroidal neovascularization (CNV), via its interaction with Tie2. To the best of our knowledge, there are no studies addressing the potential use of APC as oBRB stabilizer and CNV inhibitor.