Contribution of E-NTPDase1 (CD39) to renal protection from ischemia-reperfusion injury.

Contribution of E-NTPDase1 (CD39) to renal protection from ischemia-reperfusion injury. Research Abstract Details 

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Contribution of E-NTPDase1 (CD39) to renal protection from ischemia-reperfusion injury. Abstract Text:

Almut Grenz,Hua Zhang,Marina Hermes,Tobias Eckle,Karin Klingel,Dan Yang Huang,Christa E ,Simon C Robson,Hartmut Osswald,Holger K Eltzschig,

Previous studies showed increased extracellular nucleotides during renal ischemia-reperfusion. While nucleotides represent the main source for extracellular adenosine and adenosine signaling contributes to renal protection from ischemia, we hypothesized a role for ecto-nucleoside-triphosphate-diphosphohydrolases (E-NTPDases) in renal protection. We used a model of murine ischemia-reperfusion and in situ ischemic preconditioning (IP) via a hanging weight system for atraumatic renal artery occlusion. Initial studies with a nonspecific inhibitor of E-NTPDases (POM-1) revealed inhibition of renal protection by IP. We next pursued transcriptional responses of E-NTPDases (E-NTPDase1-3, and 8) to renal IP, and found a robust and selective induction of E-NTPDase1/CD39 transcript and protein. Moreover, based on clearance studies, plasma electrolytes, and renal tubular histology, IP protection was abolished in gene-targeted mice for cd39 whereas increased renal adenosine content with IP was attenuated. Furthermore, administration of apyrase reconstituted renal protection by IP in cd39-/- mice. Finally, apyrase treatment of wild-type mice resulted in increased renal adenosine concentrations and a similar degree of renal protection from ischemia as IP treatment. Taken together, these data identify CD39-dependent nucleotide phosphohydrolysis in renal protection. Moreover, the present studies suggest apyrase treatment as a novel pharmacological approach to renal diseases precipitated by limited oxygen availability.

Contribution of E-NTPDase1 (CD39) to renal protection from ischemia-reperfusion injury. Publishing Authors By Initials

A Grenz,H Zhang,M Hermes,T Eckle,K Klingel,DY Huang,CE ,SC Robson,H Osswald,HK Eltzschig,

For similar cardiovascular diseases: vascular diseases: reperfusion injury research abstracts see: cardiovascular diseases: vascular diseases: reperfusion injury research

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Contribution of E-NTPDase1 (CD39) to renal protection from ischemia-reperfusion injury. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: The FASEB journal : official publication of the Fe

VOLUME: 21

Page Numbers: 2863-73

Journal Abbreviation: FASEB J.

ISSN: 1530-6860

DAY: 18

MONTH: 04

YEAR: 2007

Contribution of E-NTPDase1 (CD39) to renal protection from ischemia-reperfusion injury. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 8804484

Contribution of E-NTPDase1 (CD39) to renal protection from ischemia-reperfusion injury. Keywords Mesh Terms:

KEYWORDS: Reperfusion Injury

MESH TERMS: prevention & control

Chemical & Substance for Abstract: Contribution of E-NTPDase1 (CD39) to renal protection from ischemia-reperfusion injury. Information

Substance Name: CD39 antigen

Registry Number: EC 3.6.1.5

Grant and Affiliation Information for Contribution of E-NTPDase1 (CD39) to renal protection from ischemia-reperfusion injury.

AFFILIATION: Department of Pharmacology and Toxicology, Tübingen University Hospital, Tübingen, Germany.

Country: United States

AGENCY: United States NHLBI

GRANT: 1P01 HL 076540

ACRONYM: HL

MEDLINETA: FASEB J

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