Key result
COX-2 inhibitors prevent intravitreal neovascularization in experimental ischemic proliferative retinopathy, unlike COX-1 inhibitors.
Why the study?
Does COX-2 inhibition prevent intravitreal neovascularization in ischemic proliferative retinopathy?
Does COX-2 inhibition prevent intravitreal neovascularization in ischemic proliferative retinopathy?
Answers are grounded in this paper and cite their sources.
COX-2 inhibition prevents intravitreal neovascularization in experimental models, suggesting it may be a therapeutic target for ischemic proliferative retinopathy such as diabetic retinopathy.
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 E2, 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. CONCLUSIONS: These findings point to an important role for COX-2 in ischemic proliferative retinopathy, as in diabetes.
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Sennlaub et al. (2003) studied Ischemic proliferative retinopathy. COX-2 inhibitors vs. COX-1 inhibitors was evaluated on Intravitreal neovascularization. Specific COX-2 inhibitors, but not COX-1 inhibitors, prevented intravitreal neovascularization in experimental models of ischemic proliferative retinopathy.
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