April 2010
Volume 51, Issue 13
ARVO Annual Meeting Abstract  |   April 2010
The Role of Adenosine in the Diabetic Retina
Author Affiliations & Notes
  • N. Fatteh
    Ophthalmology, Medical College of Georgia, Augusta, Georgia
  • A. Ibrahim
    Ophthalmology, Medical College of Georgia, Augusta, Georgia
  • G. Liou
    Ophthalmology, Medical College of Georgia, Augusta, Georgia
  • Footnotes
    Commercial Relationships  N. Fatteh, None; A. Ibrahim, None; G. Liou, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 5085. doi:
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      N. Fatteh, A. Ibrahim, G. Liou; The Role of Adenosine in the Diabetic Retina. Invest. Ophthalmol. Vis. Sci. 2010;51(13):5085.

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

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Purpose: : Recent evidence has indicated that adenosine can regulate retinal immune cell function and barrier function of retinal vasculature. Therefore, understanding the mechanism of this regulation may provide a use for targeted intervention in diabetic retinopathy. Ischemic stress in the diabetic retina is known to activate microglia, cause neuronal cell death, and breakdown of the blood-retinal barrier. Ischemic stress also causes the release of adenosine through the bi-directional equilibrative nucleoside transporters (ENT). Extracellular adenosine is known to attenuate inflammation by activating A2a receptor, and A2a receptor-selective agonists have been shown to be effective in anti-inflammation in acute or chronic inflammatory diseases. In high glucose-treated cardiac fibroblasts, however, decreased adenosine release and uptake were measured in comparison to low glucose-treated cells. This suggests impairment in the function of ENT and the subsequent adenosine-A2a receptor signaling in diabetes. This study is the first step to test the hypothesis that the anti-inflammatory function of adenosine-A2a receptor signaling is impaired in the diabetic retina.

Methods: : Primary cultures of rat retinal microglial cells were treated with or without Amadori-glycated albumin (AGA), which has been implicated as a causal factor in diabetic complications. TNF-α levels in the media were measured by ELISA. Adenosine uptake by microglial cells was determined within one minute after the addition of [2-3H] adenosine. Washed cells were solubilized and radioactivity quantified. For adenosine release, cellular ATP was labeled with [8-14C] adenine, and ATP was depleted in the presence of 2-deoxyglucose and antimycin A. At appropriate time points within 15 minutes of ATP depletion, medium aliquots containing released adenosine was separated on silica gel plate and quantified.

Results: : Retinal microglial cells showed a significant increase in TNF-α release after AGA treatment. Adenosine uptake and release by these cells were inhibited by AGA treatment.

Conclusions: : These results suggest that cell protection mechanisms effected by adenosine are impaired in the diabetic retina. Activation of A2a receptor by a selective agonist, as shown in other organ systems, may be effective in anti-inflammation in the diabetic retina.

Keywords: diabetic retinopathy • adenosine • inflammation 

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