March 2012
Volume 53, Issue 14
ARVO Annual Meeting Abstract  |   March 2012
Effects Of Aldose Reductase Deletion On Diabetes -induced Retinal Inflammation and Vascular Degeneration
Author Affiliations & Notes
  • Jie Tang
    Medicine and Center for Diabetes Research,
    Case Western Reserve Univ, Cleveland, Ohio
  • Mark Petrash
    Ophthalmology, University of Colorado, Denver, Colorado
  • Timothy S Kern
    Medicine and Center for diabetes Research,
    Case Western Reserve Univ, Cleveland, Ohio
  • Footnotes
    Commercial Relationships  Jie Tang, None; Mark Petrash, None; Timothy S Kern, None
  • Footnotes
    Support  NIH Grant
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 2425. doi:
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      Jie Tang, Mark Petrash, Timothy S Kern; Effects Of Aldose Reductase Deletion On Diabetes -induced Retinal Inflammation and Vascular Degeneration. Invest. Ophthalmol. Vis. Sci. 2012;53(14):2425.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: : Aldose reductase (AR) and inflammation have been implicated in the pathogenesis of diabetic retinopathy. The aim of this study was to investigate effects of aldose reductase deletion on diabetes-induced inflammatory changes in the retina, and on vascular pathology

Methods: : Wild-type (C57BL/6J) and aldose reductase (AR) deficient mice were made diabetic with streptozotocin. Mice were sacrificed at 2 mos and 10 mos of study to evaluate retinal vascular histopathology (elastase digestion), as well as parameters of oxidative stress (retinal superoxide) and inflammation (expression of inflammatory proteins).

Results: : Wild-type mice diabetic for 10 mos developed the expected degeneration of retinal capillaries, and diabetes of 2 mos duration increased both superoxide production and expression of iNOS and ICAM. Co-culture of endothelial cells with leukocytes from wildtype diabetics killed more endothelial cells than did leukocytes from nondiabetics. Deletion of AR resulted in total suppression of the diabetes-induced increase in expression of iNOS and generation of retinal superoxide, and partial inhibition of vascular histopathology. Neither leukocyte-mediated killing of endothelial cells or increased expression of ICAM, however, were corrected in AR-deficient diabetic mice.

Conclusions: : AR regulates the diabetes-induced increase in superoxide generation by the retina, and regulate some, but not all, aspects of the diabetes-induced inflammation and capillary degeneration.

Keywords: diabetic retinopathy • pathology: experimental • inflammation 

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