alexa Thrombospondin-1 Deficiency Exacerbates the Pathogenesi
ISSN: 2155-6156

Journal of Diabetes & Metabolism
Open Access

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Research Article

Thrombospondin-1 Deficiency Exacerbates the Pathogenesis of Diabetic Retinopathy

Christine M Sorenson1,5*, Shoujian Wang2, Robert Gendron3, Hélène Paradis3 and Nader Sheibani2,4,5

1Department of Pediatrics, University of Wisconsin School of Medicine and Public Health, USA

2Department of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health, USA

3Memorial University of Newfoundland, St. John’s, Canada, USA

4Department of Pharmacology, University of Wisconsin School of Medicine and Public Health, USA

5McPherson Eye Research Institute, University of Wisconsin School of Medicine and Public Health, USA

Corresponding Author:
Christine M Sorenson
Department of Pediatrics, University of Wisconsin
School of Medicine and Public Health, 600 Highland Avenue
H4/444 CSC, Madison, WI 53792-4108, USA
Tel: 608-263-5831
Fax: 608-265-3397
E-mail: [email protected]

Received Date: March 14, 2013; Accepted Date: May 20, 2013; Published Date: May 25, 2013

Citation: Sorenson CM, Wang S, Gendron R, Paradis H, Sheibani N (2013) Thrombospondin-1 Deficiency Exacerbates the Pathogenesis of Diabetic Retinopathy. J Diabetes Metab S12:005. doi: 10.4172/2155-6156.S12-005

Copyright: © 2013 Sorenson CM, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Abstract

Diabetic retinopathy is a leading cause of blindness in the United States. Access to new animal models that exhibit retinal vasculopathies with short duration of diabetes, are vital for understanding the underlying mechanisms and examining the efficacy of new treatment modalities. Our previous studies demonstrated decreased expression of Thrombospondin-1 (TSP1), an endogenous inhibitor of angiogenesis, in eyes from both patients and rodents with diabetes. Here we examined whether TSP1 deficiency could exacerbate diabetic retinal vasculopathies. Akita/+ male mice reproducibly develop diabetes by 4 weeks of age. These mice demonstrated the early non-proliferative stages of diabetic retinopathy, including decreased numbers of pericytes and increased glial cell activation. However, Akita/+ male mice deficient in TSP1 (Akita/+; TSP1-/-) demonstrated more advanced stages of diabetic retinopathy with a 4-fold increase in acellular capillaries and increased fibronectin and GFAP expression. These vascular changes were not attributable to aberrant retinal vascular development in the absence of TSP1, since down-regulation of TSP1 postnatally in the endothelium also resulted in more severe retinopathy. In addition, lack of another endogenous inhibitor of angiogenesis, pigment epithelium derived factor (PEDF), also enhanced diabetic retinopathy in Akita/+ mice. Akita/+; PEDF-/- male mice demonstrated increased numbers of acellular capillaries compared to controls but at a level lower than that observed in Akita/+; TSP1-/- mice. Thus, the exacerbation of diabetic retinopathy in Akita/+; TSP1-/- mice will allow the study of retinal vasculopathies with a shorter duration of diabetes and facilitate future testing of treatment modalities that protect the retinal vasculature and preserve sight.

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