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Brian C. Oveson, Takeshi Iwase, Sean Hackett, Christopher Seidel, Nathan L. Mata, Peter A. Campochiaro; Fenretinide Prevents Retinal Neovascularization in Mouse Models of Angiogenesis. Invest. Ophthalmol. Vis. Sci. 2012;53(14):2994.
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To assess the effects of fenretinide treatment in mouse models of choroidal and retinal neovascularization (NV).
Four week-old C57Bl/6 mice received either fenretinide-supplemented or control diet for four weeks before and 2 weeks after rupture of Bruch’s membrane by laser photocoagulation and then the area of choroidal neovascularization (CNV) at rupture sites was measured. Pregnant C57Bl/6 mice were given fenretinide-supplemented or control diet starting 1 week before giving birth. Oxygen-induced ischemic retinopathy was induced in the pups and the area of retinal NV was measured at P17. Pregnant rho/VEGF mice were given fenretinide-supplemented or control diet starting 1 week before giving birth. At P28, the pups were perfused with fluorescein-labeled dextran and the area of NV per retina was measured.
Compared to controls, fenretinide-treated mice had a significant reduction in the area of CNV at Bruch’s membrane rupture sites (0.003+0.0004 vs 0.006+0.0009 mm2; p<0.002). Fenretinide-treated mice also had a significant reduction in ischemia-induced retinal NV (0.012+0.004 vs 0.032+0.003 mm2; p<0.001). This was associated with a significant reduction in the number of macrophages in ischemic retina. In rho/VEGF transgenic mice, fenretinide treatment significantly reduced the area of subretinal NV per eye (0.004+0.0009 vs 0.018+0.003 mm2; p<0.001).
Fenretinide reduces macrophage influx into the retina and suppresses retinal and choroidal NV.
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