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Publication : Reduced choroidal neovascular membrane formation in cyclooxygenase-2 null mice.

First Author  Rezaei KA Year  2011
Journal  Invest Ophthalmol Vis Sci Volume  52
Issue  2 Pages  701-7
PubMed ID  20881304 Mgi Jnum  J:171554
Mgi Id  MGI:4950349 Doi  10.1167/iovs.10-6319
Citation  Rezaei KA, et al. (2011) Reduced choroidal neovascular membrane formation in cyclooxygenase-2 null mice. Invest Ophthalmol Vis Sci 52(2):701-7
abstractText  PURPOSE: To assess the degree of laser-induced choroidal neovascular membrane formation in wild-type (WT) and COX-2 null mice and to measure vascular endothelial growth factor (VEGF), interleukin (IL)-1beta, and tumor necrosis factor (TNF)-alpha levels in the retina and choroid. METHODS: Four laser burns were placed in each eye of WT and COX-2 null mice to induce choroidal neovascularization. Fluorescein angiography (FA) was performed at 14 days, and retinal pigment epithelium-choroid-sclera (choroidal) flat mounts were prepared. The retina and choroid were isolated from WT and COX-2 null mice at 24, 72, and 168 hours after laser photocoagulation and from unlasered eyes and were tested for VEGF, IL-1beta, and TNF-alpha. RESULTS: COX-2 null mice demonstrated 58% (P = 0.001) and 48% (P = 0.001) reductions in CNV formation on FA and choroidal flat mounts, respectively, compared with WT mice. For unlasered mice, mean VEGF concentrations in the retina and choroid were 1.2 +/- 0.42 pg/mg protein for WT but only 0.42 +/- 0.2 pg/mg protein for COX-2 null mice (P < 0.05). After laser photocoagulation, WT mice showed significantly greater VEGF and IL-beta expression in the retina and choroid by 168 hours (P < 0.05) and 72 hours (P < 0.05), respectively, compared with COX-2 null mice. CONCLUSIONS: COX-2 null mice exhibited significantly less choroidal neovascular membrane formation associated with reduced expression of VEGF. The results of this study suggest that COX-2 modulates VEGF expression in CNV and implicates a potential therapeutic role for nonsteroidal anti-inflammatory drugs.
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