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Cyclooxygenase-2 in human and experimental ischemic proliferative retinopathy.

Abstract : 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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Contributor : Florian Sennlaub Connect in order to contact the contributor
Submitted on : Friday, January 15, 2010 - 9:56:07 AM
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Florian Sennlaub, Fatemeh Valamanesh, Alejandro Vazquez-Tello, Ahmed M. El-Asrar, Daniella Checchin, et al.. Cyclooxygenase-2 in human and experimental ischemic proliferative retinopathy.. Circulation, American Heart Association, 2003, 108 (2), pp.198-204. ⟨10.1161/01.CIR.0000080735.93327.00⟩. ⟨inserm-00150824⟩



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