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J. F. McGinnis, X. Zhou, L. Kong, S. Sezate, S. Seal, L. L. Wong; Therapeutic Treatment of Retinal Angiomatous Proliferation in the vldlr(-/-) Mutant Mouse Using Nanoceria. Invest. Ophthalmol. Vis. Sci. 2009;50(13):1194.
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© ARVO (1962-2015); The Authors (2016-present)
To test the hypothesis that the retinal lesions in the vldlr(-/-) mouse are mediated by Reactive Oxygen Species and that the Nanoceria, by catalytically destroying Reactive Oxygen Species, can prevent CNV and retinal vascular angiogenesis in the outer nuclear layer.
Nanoceria were injected intravitreally into vldlr(-/-) eyes at postnatal day 7 and the mice were killed at P14, 21, 28 or 35. Dextran conjugated fluorescein and confocal microscopy were used to visualize the choroidal and retinal vasculature. Some mice were injected with Nanoceria on day 28, after the vascular lesions had already formed, and killed one or two weeks later. Cellular oxidation by Reactive Oxygen Species was visualized using a dichlorofluorescein imaging assay. Vascular Endothelial Growth Factor (VEGF) was assayed by Western blots and immunocytochemistry.
CNV, retinal vascular lesions, Reactive Oxygen Species and VEGF increase in the vldlr(-/-) retina during development from P7 to P35 and all of these increases are inhibited by a single injection of Nanoceria at P7. VEGF, retinal lesions and CNV present prior to injection, significantly regressed within one week of injection of Nanoceria. VEGF in the outer nuclear layer was shown to be present in the photoreceptor cells. ROS were shown to be concentrated in regions where vascular lesions were forming.
Because the therapeutic use of nanoceria significantly inhibits development and maintenance of the mutant retinal phenotype of the vldlr(-/-) mouse, we conclude that the Nanoceria may be just as effective in treating CNV, retinal vascular lesions and retinal degeneration in patients with Retinal Angiomatous Proliferation.
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