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Loss of CD40 attenuates experimental diabetes-induced retinal inflammation but does not protect mice from electroretinogram defects

Published online by Cambridge University Press:  27 June 2017

IVY S. SAMUELS
Affiliation:
Research Service, Louis Stokes Cleveland Veterans Administration Medical Center, Cleveland, Ohio 44106 Department of Ophthalmic Research, Cole Eye Institute, Cleveland, Ohio 44195
JOSE-ANDRES C. PORTILLO
Affiliation:
Division of Infectious Diseases and HIV Medicine, Department of Medicine, Case Western Reserve University, Cleveland, Ohio 44106
YANLING MIAO
Affiliation:
Division of Infectious Diseases and HIV Medicine, Department of Medicine, Case Western Reserve University, Cleveland, Ohio 44106
TIMOTHY S. KERN
Affiliation:
Research Service, Louis Stokes Cleveland Veterans Administration Medical Center, Cleveland, Ohio 44106 Department of Ophthalmology and Visual Sciences, Case Western Reserve University, Cleveland, Ohio 44106 Department of Pharmacology, Case Western Reserve University, Cleveland, Ohio 44106
CARLOS S. SUBAUSTE
Affiliation:
Division of Infectious Diseases and HIV Medicine, Department of Medicine, Case Western Reserve University, Cleveland, Ohio 44106 Department of Ophthalmology and Visual Sciences, Case Western Reserve University, Cleveland, Ohio 44106 Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106

Abstract

Chronic low grade inflammation is considered to contribute to the development of experimental diabetic retinopathy (DR). We recently demonstrated that lack of CD40 in mice ameliorates the upregulation of inflammatory molecules in the diabetic retina and prevented capillary degeneration, a hallmark of experimental diabetic retinopathy. Herein, we investigated the contribution of CD40 to diabetes-induced reductions in retinal function via the electroretinogram (ERG) to determine if inflammation plays a role in the development of ERG defects associated with diabetes. We demonstrate that diabetic CD40−/− mice are not protected from reduction to the ERG b-wave despite failing to upregulate inflammatory molecules in the retina. Our data therefore supports the hypothesis that retinal dysfunction found in diabetics occurs independent of the induction of inflammatory processes.

Type
Research Article
Copyright
Copyright © Cambridge University Press 2017 

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Footnotes

*

These authors contributed equally to this work.

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