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- Title
Ccl2/Cx3cr1-Deficient Mice: An Animal Model for Age-Related Macular Degeneration.
- Authors
Chi-Chao Chan; Ross, Robert J.; Defen Shen; Xiaoyan Ding; Majumdar, Zigurts; Bojanowski, Christine M.; Min Zhou; Salem Jr., Norman; Bonner, Robert; Jingsheng Tuo
- Abstract
Background/Aims: Senescent Ccl2-/- mice develop cardinal features of human age-related macular degeneration (AMD). Loss-of-function single-nucleotide polymorphisms within CX3CR1 are associated with AMD. Methods: We generated Ccl2-/-/Cx3cr1-/- [double-knockout (DKO)] mice and evaluated the eyes using fundoscopy routine histology, immunochemistry, biochemistry and proteomics. Results: At 6 weeks old, all DKO mice developed AMD-like retinal lesions such as abnormal retinal pigment epithelium cells, drusen, photoreceptor atrophy and choroidal neovascularization, which progressed with age and reversed with high omega-3 long-chain polyunsaturated fatty acid diet. N-retinylidene-N-retinylethanolamine (A2E), a major lipofuscin fluorophore, illustrated by an emission peak at ∼600 nm, was significantly higher in DKO retinal pigment epithelium. Decreased ERp29 was found in the retina of DKO mice. Conclusion: A broad spectrum of AMD pathologies with early onset and high penetrance in these mice implicate certain chemokines, A2E and endoplasmic reticulum proteins in AMD pathogenesis. Copyright © 2008 S. Karger AG, Basel
- Subjects
LABORATORY mice; ANIMAL models of retinal degeneration; MOLECULAR chaperones; FATTY acids; UNSATURATED fatty acids
- Publication
Ophthalmic Research, 2008, Vol 40, Issue 3/4, p124
- ISSN
0030-3747
- Publication type
Article
- DOI
10.1159/000119862