Evidence map›Paper›PMID 12939345›Full record

ArticleThe Journal of experimental medicine2003

Coordinated adenine nucleotide phosphohydrolysis and nucleoside signaling in posthypoxic endothelium: role of ectonucleotidases and adenosine A2B receptors.

Holger K Eltzschig, Juan C Ibla, Glenn T Furuta, Martin O Leonard, Kenneth A Jacobson, Keiichi Enjyoji, Simon C Robson, Sean P Colgan

Open access · greenAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 282 papers.

0numbers the graph read from it
0cells of the map it votes in
282citing papers in PubMed
8.7field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

282 citing papers in PubMed, 493 citations in OpenAlex.

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222 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 6 institutions in 3 countries.

Holger K EltzschigCenter for Experimental Therapeutics and Reperfusion Injury, Brigham and Women's Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA.
Juan C Ibla
Glenn T Furuta
Martin O Leonard
Kenneth A Jacobson
Keiichi Enjyoji
Simon C Robson
Sean P Colgan
Beth Israel Deaconess Medical Center · USBrigham and Women's Hospital · USBoston Children's Hospital · USNational Institutes of Health · USStanford University · USUniversity College Dublin · IE

Funding

Novel anti-inflamatory lipid mediatorsP01DE013499 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI SERHAN, CHARLES NICHOLAS · 2000 to 2004
$5.3M
ROLE OF EPITHELIA IN ISCHEMIA/REPERFUSION INJURYR01DK050189 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI COLGAN, SEAN P · 2000 to 2024
$5.0M
Hypoxia, HIF, and Mucosal InflammationR37DK050189 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI COLGAN, SEAN P · 2010 to 2019
$4.1M
Neutrophils and Vascular Endothelial PermeabilityR01HL060569 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI COLGAN, SEAN P · 1999 to 2013
$3.5M
Drugs that Act at Adenosine ReceptorsZ01DK031117 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI JACOBSON, KENNETH ALAN · 1991 to 2008
$854k
PROSTHETIC GROUPS FOR RADIOLABELING OF FUNCTIONALIZED DRUGS AND PEPTIDESZ01DK031116 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI JACOBSON, KENNETH ALAN · 1991 to 2008
$769k
EPITHELIA AND ISCHEMIA/REPERFUSION INJURYR29DK050189 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI COLGAN, SEAN P · 1995 to 1999
–
Intramural NIH HHS Z01 DK031116NHLBI NIH HHS HL 60569NHLBI NIH HHS R01 HL060569NIDCR NIH HHS DE 13499NIDCR NIH HHS P01 DE013499NIDDK NIH HHS DK 50189NIDDK NIH HHS R01 DK050189NIDDK NIH HHS R29 DK050189NIDDK NIH HHS R37 DK050189
6 · The paper itself

Abstract

Limited oxygen delivery to tissues (hypoxia) is common in a variety of disease states. A number of parallels exist between hypoxia and acute inflammation, including the observation that both influence vascular permeability. As such, we compared the functional influence of activated polymorphonuclear leukocytes (PMN) on normoxic and posthypoxic endothelial cells. Initial studies indicated that activated PMN preferentially promote endothelial barrier function in posthypoxic endothelial cells (>60% increase over normoxia). Extension of these findings identified at least one soluble mediator as extracellular adenosine triphosphate (ATP). Subsequent studies revealed that ATP is coordinately hydrolyzed to adenosine at the endothelial cell surface by hypoxia-induced CD39 and CD73 (>20-and >12-fold increase in mRNA, respectively). Studies in vitro and in cd39-null mice identified these surface ecto-enzymes as critical control points for posthypoxia-associated protection of vascular permeability. Furthermore, insight gained through microarray analysis revealed that the adenosine A2B receptor (AdoRA2B) is selectively up-regulated by hypoxia (>5-fold increase in mRNA), and that AdoRA2B antagonists effectively neutralize ATP-mediated changes in posthypoxic endothelial permeability. Taken together, these results demonstrate transcription coordination of adenine nucleotide and nucleoside signaling at the vascular interface during hypoxia.

Indexed as

Adenine NucleotidesAdenosineAdenosine TriphosphatasesAntigens, CDApyraseBase SequenceCell HypoxiaCell Membrane PermeabilityCells, CulturedDNA PrimersEndothelium, VascularHumansHydrolysisKineticsMicrocirculationNeutrophil ActivationAdenine NucleotidesAdenosineAdenosine TriphosphatasesAntigens, CDApyraseCD39 antigenDNA Primersectonucleotide pyrophosphohydrolasePyrophosphatasesReceptor, Adenosine A2BReceptors, Purinergic P1

Identifiers

PMID12939345
PMCPMC2194189
OpenAlexW2138216041

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.