CD73 protects kidney from ischemia-reperfusion injury through reduction of free radicals
Article first published online: 11 NOV 2011
© 2011 The Authors. APMIS © 2011 APMIS
Volume 120, Issue 2, pages 130–138, February 2012
How to Cite
JIAN, R., SUN, Y., WANG, Y., YU, J., ZHONG, L. and ZHOU, P. (2012), CD73 protects kidney from ischemia-reperfusion injury through reduction of free radicals. APMIS, 120: 130–138. doi: 10.1111/j.1600-0463.2011.02827.x
- Issue published online: 10 JAN 2012
- Article first published online: 11 NOV 2011
- Received 22 February 2011. Accepted 30 August 2011
- complement activation;
- free radicals
Jian R, Sun Y, Wang Y, Yu J, Zhong L, Zhou P. CD73 protects kidney from ischemia-reperfusion injury through reduction of free radicals. APMIS 2011.
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.