Journal
APMIS
Volume 120, Issue 2, Pages 130-138Publisher
WILEY
DOI: 10.1111/j.1600-0463.2011.02827.x
Keywords
CD73; adenosine; complement activation; free radicals
Categories
Funding
- National Natural Science Foundation of China [30971163]
- National 863 subproject [2007AA021809]
- Science and Technology Commission of Shanghai [0852nm04400]
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Renal ischemia-reperfusion injury (IRI) may cause severe systemic diseases. Extracellular adenosine is anti-inflammatory especially during hypoxemia. As ecto-5-nucleotidase (CD73) is the rate-limiting enzyme for extracellular adenosine generation, it may protect renal IRI through adenosine production. In the current studies, we investigated the effects of CD73 in genetically modified mice. We found that renal IRI caused more serious histological injury, vascular permeability, and lipid peroxidation in CD73-/-) than that in CD73 +/+ mice. In addition, AMP and free radical concentrations were much higher in CD73-/-) than that in CD73 +/+ mice. Our data support the fact that CD73 may protect the kidney from IRI through adenosine production and a reduction of free radicals.
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