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I. Chowers, E. Feldmesser, A. Obolensky, F. Sennlaub, E. Banin, D. J. Zack, S. Horowitz; Further Characterization of Retinal Alterations in the Chemokine Receptor Type 2 (CCR2) Deficient Mice. Invest. Ophthalmol. Vis. Sci. 2009;50(13):1935.
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The CCR2 deficient mouse was reported to manifest retinal alterations which share similarities with age related macular degeneration (AMD) in humans. We aim to further characterize retinal alterations in this mouse strain and to evaluate its similarities to the human disease.
CCR2 deficient mice and age and genetic background matched wild type mice (WT) were studied. Mice were evaluated at the age of 7, 12, and 16-23 months by ophthalmoscopy, fundus photography, conventional histology, electroretinography (ERG), immunohistochemistry, and microarray and quantitative real time RT-PCR (QPCR) analyses of gene expression.
At 16-23 months of age CCR2 deficient mice showed fundoscopic lesions reminiscence of drusen which were 5.2-fold more frequent than in WT mice as assessed by masked observer (p=0.0004). CCR2 deficient retinas also showed 2-fold higher autofluorescence levels compared with WT mice (p= 0.02). While drusen were not identified in sequential histological sectioning of CCR2 deficient mice eyes their subretinal space was enriched with microglial cells. ERG responses and retina thickness were similar in CCR2 deficient and WT mice, but, immunostaining intensity for rhodopsin was 1.2-fold lower in CCR2 deficient mice (p=0.04). Microarray and QPCR analyses revealed altered expression of genes belonging to several functional classes among them immune response and shared similarities with gene expression signature of other mice models for retinal degeneration.
Aged CCR2 deficient mice show retinal alterations. While drusen are not a common histological finding in these mice, fundoscopic drusen-like lesions are often observed and are associated with altered retinal immune response. Combined with previous studies these data suggest that drusen are not required for development of retinal alterations associated with the perturbed immune response and complement activation present in this mouse strain.
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