Deficiency or inhibition of CD73 protects in mild kidney ischemia-reperfusion injury

SV Rajakumar; B Lu; S Crikis; SC Robson; AJF D'Apice; PJ Cowan; KM Dwyer

Journal article

Deficiency or inhibition of CD73 protects in mild kidney ischemia-reperfusion injury

SV Rajakumar, B Lu, S Crikis, SC Robson, AJF D'Apice, PJ Cowan, KM Dwyer

Transplantation | LIPPINCOTT WILLIAMS & WILKINS | Published : 2010

DOI: 10.1097/TP.0b013e3182003d9b

Abstract

Background. Adenosine agonists are protective in numerous models of ischemia-reperfusion injury (IRI). Pericellular adenosine is generated by the hydrolysis of extracellular adenosine triphosphate and adenosine diphosphate by the ectonucleotidase CD39 and the subsequent hydrolysis of adenosine monophosphate (AMP) by the ectonucleotidase CD73. CD39 activity is protective in kidney IRI, whereas the role of CD73 remains unclear. Methods. Wild-type (WT), CD73-deficient (CD73KO), CD39-transgenic (CD39tg), and hybrid CD39tg.CD73KO mice underwent right nephrectomy and unilateral renal ischemia (18-min ischemia by microvascular pedicle clamp). Renal function (serum creatinine [SCr], micromolar per l..

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University of Melbourne Researchers

Peter Cowan Author

Karen Dwyer Author

Grants

Awarded by National Heart, Lung, and Blood Institute

Funding Acknowledgements

This work was supported by the NHMRC (Australia), Genzyme Renal Innovations Program (K.M.D.), NIH (S.C.R.), and a Kidney Health Australia research scholarship (S.V.R.).