Cyclooxygenase-2 in human and experimental ischemic proliferative retinopathy.

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2003

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info:eu-repo/semantics/altIdentifier/doi/10.1161/01.CIR.0000080735.93327.00

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info:eu-repo/semantics/altIdentifier/pmid/12821538

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info:eu-repo/semantics/altIdentifier/eissn/1524-4539

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info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_3A50A6EB875D1

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Angiogenesis

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F. Sennlaub et al., « Cyclooxygenase-2 in human and experimental ischemic proliferative retinopathy. », Serveur académique Lausannois, ID : 10.1161/01.CIR.0000080735.93327.00


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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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