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Norihito Fujita, Shuko Nishimoto, Takeshi Miyamoto, Yuka Okada, Shizuya Saika; Loss Of Nitric Oxide Synthase Type Ii Inhibits Ocular Neovascularization In Mice; Corneal Neovascularization And Argon Laser-induced Choroidal Neovascularization. Invest. Ophthalmol. Vis. Sci. 2011;52(14):6402.
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To evaluate the effects of lacking nitric oxide synthase type II (NOS2) on neovascular disease models, corneal neovascularization and experimental laser induced-choroidal neovascularization (CNV), in mice. CNV is a major feature of the exudative form of age-related macular degeneration (AMD).
(1) Neovascularization in the peripheral corneal stroma was induced in C57BL/6-background NOS2-null mice (KO, n = 6) or wild-type mice (WT, n = 6) by cauterization at the central cornea. Cryosection was examined with CD31-immunohistochemistry at day 7. The length of new vessels in the stroma from the anterior chamber angle was measured. (2) CNV was induced in an eye of KO or WT mice (n = 10 in each genotype) by Argon laser irradiation (100 mW, 0.10 sec, ϕ 100 µm). Fourteen days after the laser irradiation, high-resolution angiography with fluorescein isothiocyanate dextran was performed and the degree of CNV formation was evaluated in using choroidal flat mounts under fluorescent microscopy.
(1) The length of corneal new vessels in KO mice was 0.227 (+/- 0.156) mm and the length of WT mice was 0.101 (+/- 0.098) mm (p < 0.05). (2) The CNV size in KO mice was 33579.1(+/- 17234.8) µm² and the CNV size in WT mice was 17642.8(+/- 7304.0) µm² (p < 0.01).
Lacking NOS2 suppresses cauterization-induced corneal neovascularization and Argon laser-induced CNV in mice. Control of nitric monoxide production might be a potential target in prevention/treatment of neovascularization-related ocular diseases.
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