Cyclooxygenase-2 in human and experimental ischemic proliferative retinopathy

Article

关键词: PLATELET-ACTIVATING-FACTOR;    OXYGEN-INDUCED RETINOPATHY;    RETINAL NEOVASCULARIZATION;    PROSTAGLANDIN E-2;    OCULAR NEOVASCULARIZATION;    GROWTH-FACTOR;    IN-VIVO;    ANGIOGENESIS;    INHIBITION;    APOPTOSIS;   

DOI  :  10.1161/01.CIR.0000080735.93327.00

来源: SCIE

【 摘 要 】

Background-Intravitreal neovascular diseases, as in ischemic retinopathies, are a major cause of blindness. Because inflammatory mechanisms influence vitreal neovascularization and cyclooxygenase (COX)-2 promotes tumor angiogenesis, we investigated the role of COX-2 in ischemic proliferative retinopathy. Methods and Results-We describe here that COX-2 is induced in retinal astrocytes in human diabetic retinopathy, in the murine and rat model of ischemic proliferative retinopathy in vivo, and in hypoxic astrocytes in vitro. Specific COX-2 but not COX-1 inhibitors prevented intravitreal neovascularization, whereas prostaglandin E-2, mainly via its prostaglandin E receptor 3 (EP3), exacerbated neovascularization. COX-2 inhibition induced an upregulation of thrombospondin-1 and its CD36 receptor, consistent with the observed antiangiogenic effects of COX-2 inhibition; EP3 stimulation reversed effects of COX-2 inhibitors on thrombospondin-1 and CD36. Conclusion-These findings point to an important role for COX-2 in ischemic proliferative retinopathy, as in diabetes.

【 授权许可】

Free