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Publication

Retinal Ion Regulation in a Mouse Model of Diabetic Retinopathy: Natural History and the Effect of Cu/Zn Superoxide Dismutase Overexpression

Authors Bruce A. Berkowitz, Marius Gradianu, David Bissig, Timothy S. Kern, Robin Roberts Submitted By Bruce Berkowitz on 12/5/2008 Status Published Journal Investigative ophthalmology & visual science Year 2008 Date Published 5/1/2009 Volume : Pages Not Specified : Not Specified PubMed Reference Abstract Purpose: To test the hypotheses that manganese-enhanced MRI (MEMRI) is useful in evaluating intraretinal ion dysregulation in wildtype and Cu/Zn superoxide dismutase (SOD1) overexpressor mice. Methods: Central intraretinal ion activity and retinal thickness were measured from high resolution data of these groups: light and dark adapted wildtype C57BL/6 (WT) mice (to gauge MEMRI sensitivity to normal visual processing in mice), and dark-adapted diabetic and non-diabetic WT and Cu/Zn superoxide dismutase overexpressor (SOD1OE) mice. Glycated hemoglobin and retinal vascular histopathology were also determined. Results: In WT mice, light adaptation reduced outer retinal manganese uptake compared with that in dark adaptation; no effect on inner retinal uptake was found. In diabetic WT mice, intraretinal manganese uptake became subnormal between 1.5 and 4 mo of diabetes and then relatively increased. Central retinal thicknesses, as determined with MEMRI, decreased as a function of age in diabetic mice but remained constant in control mice. Non-diabetic SOD1OE mice had normal retinal manganese uptake but subnormal retinal thickness and supernormal acellular capillary density. At 4.2 mo of diabetes, SOD1OE mice had normal manganese uptake and no further thinning; acellular capillaries frequency did not increase by 9-10 mo of diabetes. Conclusions: In emerging diabetic retinopathy, MEMRI provided an analytic measure of an ionic dysregulatory pattern that was sensitive to SOD1 overexpression. The potential benefit of SOD1 overexpression to inhibit retinal pathology in this model is limited by the retinal and vascular degeneration that develops independently of diabetes.

Investigators with authorship
Name Institution Bruce Berkowitz Wayne State University

Complications
All ComplicationsBioinformatics BoneCardiomyopathy CardiovascularGastro-Intestinal (GI) NephropathyNeuropathy & Neurocognition Pediatric Endocrinology Retinopathy UropathyWound Healing

Genes
Symbol Description Sod1 superoxide dismutase 1, soluble