Ccl2/Cx3cr1 knockout mice have inner retinal dysfunction but are not an accelerated model of AMD

KA Vessey; U Greferath; AI Jobling; JA Phipps; T Ho; M Waugh; EL Fletcher

Journal article

Ccl2/Cx3cr1 knockout mice have inner retinal dysfunction but are not an accelerated model of AMD

KA Vessey, U Greferath, AI Jobling, JA Phipps, T Ho, M Waugh, EL Fletcher

Investigative Ophthalmology and Visual Science | ASSOC RESEARCH VISION OPHTHALMOLOGY INC | Published : 2012

DOI: 10.1167/iovs.12-10650

Abstract

Purpose. The chemokine, Ccl2, and the fractalkine receptor, Cx3cr1, have both been implicated in the pathogenesis of age related macular degeneration (AMD), with mice lacking both genes exhibiting features of AMD by 3 months of age. However, recent reports indicate that this ascribed phenotype is due to the presence of a retinal degeneration mutation (crb1rd8/rd8, rd8) on the background strain. Our aim was to characterize the retinal effects of lack of Ccl2 and Cx3cr1 (Ccl2-/-/Cx3cr1EGFP/EGFP, CDKO-mice), in mice without the rd8 mutation. Methods. Nine-month-old, CDKO and wildtype C57blk6J mice were investigated for retinal fundus appearance and histology. The function of the rod and cone pa..

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University of Melbourne Researchers

Kirstan Vessey Author

Una Greferath Author

Andrew Jobling Author

Erica Fletcher Author

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Grants

Awarded by NHMRC

Funding Acknowledgements

Supported by the NHMRC project Grants 566814 and 1021918 (ELF); by the American Health Assistance Foundation; Macular Degeneration Research grant (ELF); and a Victoria's Science Agenda grant (ELF).