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We investigated the human apolipoprotein E2(apoE2) transgenic mouse as an animal model system for age-related macular degeneration (AMD). Transgenic mice expressinghuman apoE2 and C57BL/6J mice were fed normal chow or ahigh-fat diet for 4 weeks. Eyes were collected from the miceand lipid deposits in retinal pigment epithelium (RPE) werevascular endothelial growth factor (VEGF), basic fibroblastgrowth factor (bFGF), and pigment-epithelium derived factor(PEDF), which are molecular markers for angiogenesis, wereasesed with imunohistochemistry. Eyes from apoE2 mice,regardles of diet, contained lipid accumulation in RPE underelectron microscopy, whereas control C57BL/6J eyes did not.Lipid acumulation was found predominantly in the RPE andthe Bruch’s membrane and increased in the eyes of apoE2mice after one month of a high-fat diet (8±2 per 50m2 fornormal chow and 1±2 per 50m2, p<0.05). ApoE expressionwas similar in the apoE2 and control mice; however, VEGFand bFGF were overexpressed in the retinal pigmentepithelium of apoE2 eyes compared with control eyes, andPEDF expression was slightly decreased. These expressionpatterns of VEGF, bFGF, and PEDF suggest angiogenesis isprogressing in apoE2 eyes. In conclusion, the eyes of apoE2 miceof AMD, making them a suitable animal model for AMD.The expression profile of VEGF and bFGF on the retinal pigmentepithelium suggests that apoE2 may induce neovascularizationby altering angiogenic cytokines.

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