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Ccl2/Cx3cr1-deficient mice: an animal model for age-related macular degeneration.

Authors :
Chan CC
Ross RJ
Shen D
Ding X
Majumdar Z
Bojanowski CM
Zhou M
Salem N Jr
Bonner R
Tuo J
Source :
Ophthalmic research [Ophthalmic Res] 2008; Vol. 40 (3-4), pp. 124-8. Date of Electronic Publication: 2008 Apr 18.
Publication Year :
2008

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.<br />Methods: We generated Ccl2-/-/Cx3cr1-/- [double-knockout (DKO)] mice and evaluated the eyes using fundoscopy routine histology, immunochemistry, biochemistry and proteomics.<br />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 approximately 600 nm, was significantly higher in DKO retinal pigment epithelium. Decreased ERp29 was found in the retina of DKO mice.<br />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.<br /> (2008 S. Karger AG, Basel.)

Details

Language :
English
ISSN :
1423-0259
Volume :
40
Issue :
3-4
Database :
MEDLINE
Journal :
Ophthalmic research
Publication Type :
Academic Journal
Accession number :
18421225
Full Text :
https://doi.org/10.1159/000119862