December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
Non-steroid Alanti-inflammatory Drugs Prevent Early Diabetic Retinopathy: Aspirinand COX-2 Inhibition Prevent Blood-retinal Barrier Breakdown and Leukocyte Adhesion Via TNF-asuppression
Author Affiliations & Notes
  • AM Joussen
    Center for Ophthalmology Dept Vitreoretinal Surgery Köln Germany
  • V Poulaki
    Retina Research Laboratory
    Massachusetts Eye and Ear Infirmary Boston MA
  • S Döhmen
    Department of Vitreoretinal Surgery Center for Ophthalmology Köln Germany
  • K Koizumi
    Department of Vitreoretinal Surgery Center for Ophthalmology Köln Germany
  • B Kirchhof
    Department of Vitreoretinal Surgery Center of Ophthalmology Köln Germany
  • AP Adamis
    Retina Reseach Laboratory
    Massachusetts Eye and Ear Infirmary Boston MA
  • Footnotes
    Commercial Relationships   A.M. Joussen, None; V. Poulaki, None; S. Döhmen, None; K. Koizumi, None; B. Kirchhof, None; A.P. Adamis, None. Grant Identification: DFG Jo 324/4-1, Juvenile Diabetes Association, NIH
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 2969. doi:
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      AM Joussen, V Poulaki, S Döhmen, K Koizumi, B Kirchhof, AP Adamis; Non-steroid Alanti-inflammatory Drugs Prevent Early Diabetic Retinopathy: Aspirinand COX-2 Inhibition Prevent Blood-retinal Barrier Breakdown and Leukocyte Adhesion Via TNF-asuppression . Invest. Ophthalmol. Vis. Sci. 2002;43(13):2969.

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

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Abstract

Abstract: : Purpose: Leukocyte adhesion to the diabetic retinal vasculature results in early blood-retinal barrier breakdown, capillary non-perfusion, and endothelial cell injury and death. Previous work has shown that intercellular adhesion molecule-1 (ICAM-1) and the leukocyte integrin CD18 are required for these processes. In this study we investigated the effect of non-steroidal antiinflammatory drugs to prevent early diabetic changes in the retina. Methods: In this study, diabetes was induced in Long Evans rats with streptozotocin, resulting in a 2- to 3-fold increase in retinal leukocyte adhesion. Neutrophil expression of the surface integrins CD11a, CD11b, and CD18 was significantly increased following one week of diabetes, as were retinal ICAM-1 levels. Animals were then treated with aspirin, a selective COX-2 inhibitor (meloxicam), or a soluble TNFa-receptor/Fc construct (TNFR-Fc, etanercept). Results: High-dose aspirin, etanercept, and high-dose meloxicam each reduced leukocyte adhesion in the diabetic retinal vasculature and suppressed blood-retinal barrier breakdown. High-dose aspirin downregulated the expression of neutrophil integrins CD11a, CD11b and CD18, whereas meloxicam and etanercept did not. High dose aspirin, etanercept and high-dose meloxicam each signficantly reduced retinal ICAM-1 expression. Aspirin and meloxicam each reduced TNFa levels in the diabetic retina. Notably, aspirin, meloxicam, or etanercept did not change retinal VEGF levels. The retinal expression of eNOS, and the DNA-binding capacity of retinal NF-kB, the latter a potential downstream mediator of TNFa activity, were increased in the diabetic retina and were potently suppressed by high-dose aspirin, etanercept and high-dose meloxicam. Lastly, high-dose aspirin suppressed Erk kinase activity, which is involved in CD18 upregulation. Conclusion: Taken together, these data identify COX-2 and TNFa as being operative in the early signature pathologies of diabetic retinopathy, a newly recognized inflammatory disease.

Keywords: 388 diabetic retinopathy • 301 ACAID • 437 inflammation 
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