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A. Chaudhuri, S. Balasubramanian, W. B. Thoreson, I. Ahmad; Examination of Visual Function, Pathology and Transcription Profiles of Retina, RPE and Choroid-Sclera Complex of Senescent Ccl2-/- and Sod1-/- Deficient Mice, Models of Age-Related Macular Degeneration. Invest. Ophthalmol. Vis. Sci. 2009;50(13):772.
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The manifestation of retinal degeneration in age related macular degeneration (AMD) is due to the abnormalities and dysfunction of RPE, Choroid and Bruch’s membrane with age. Emerging evidence suggests that immunity and oxidative stress plays an important role in AMD and exemplified by AMD pathogenesis displayed in mice lacking Ccl2-/- and Sod1-/- respectively. To get insights into distal mechanism(s) that leads to dysfunctions and degeneration, which may help in designing a cell- and/or small molecule based therapeutic approach we have begun analyses visual functions and pathology in conjunction with transcription profiles of affected ocular tissues in senescent Ccl2-/- andSod1-/- deficient mice.
The study consisted of 16-20 months old Ccl2-/- and Sod1-/- deficient mice and age-matched controls. Functional tests involved the examination of visual acuity by head tracking to moving stripes (optokinetic analysis) and retinal function by electroretinogram (ERG) recording. Pathological examination included morphological and immunohistochemical analyses of choroid-sclera complex, RPE and retina. Transcription profiling involved RNA extracted from retina, RPE and choroid-sclera complex using Affymetrix microarray chips.
Visual acuity was severely and significantly affected in Sod1-/- and more so in Ccl2-/- deficient mice, compared to the age matched control. Preliminary data demonstrate amplitude loss in the dark and light adapted ERG responses and differences in transcription profiles in knockout mice, compared to age-matched controls.
The visual function is compromised in both senescent models of AMD. Information about relative transcription profiles and associated signaling pathways in these AMD models will be presented.
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