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Updated: Aug 6, 2026
Assessment of Vascular Regeneration in the CNS Using the Mouse Retina
Published on: June 23, 2014
Cyclooxygenase-2 in human and experimental ischemic proliferative retinopathy
F Sennlaub1, F Valamanesh, A Vazquez-Tello
1Department of Pediatrics, Centre de Recherche, Hôpital Sainte-Justine, 3175, chemin de la Côte-Sainte-Catherine, Montréal, Québec, Canada H3T 1C5. fsennlaub@justine.umontreal.ca
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.
