Evidence map›Paper›PMID 28377485›Full record

ArticleCirculation2017

Ischemic Cerebroprotection Conferred by Myeloid Lineage-Restricted or Global CD39 Transgene Expression.

Amy E Baek, Nadia R Sutton, Danica Petrovic-Djergovic, Hui Liao, Jessica J Ray, Joan Park, Yogendra Kanthi, David J Pinsky

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Circulation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
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  4. Article
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  6. Article
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  9. Article
  10. Review
  11. Neutrophils: As a Key Bridge between Inflammation and Thrombosis.Evidence-based complementary and alternative medicine : eCAM · 2022
    Review
  12. Review
  13. Review
  14. Review
  15. CD73 Promotes Age-Dependent Accretion of Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2020
    Article
  16. The post-cardiac arrest syndrome: A case for lung-brain coupling and opportunities for neuroprotection.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019
    Review
  17. Review
  18. CD39 AS A CRITICAL ECTONUCLEOTIDASE DEFENSE AGAINST PATHOLOGICAL VASCULAR REMODELING.Transactions of the American Clinical and Climatological Association · 2018
    Article
  19. Article
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 1 institution in 1 country.

Amy E BaekFrom Department of Molecular and Integrative Physiology (A.E.B., D.J.P.) and Department of Internal Medicine (N.R.S., D.P.-D, H.L., J.R., Y.K., D.J.P.), Division of Cardiovascular Medicine University of Michigan Medical Center, Ann Arbor; and Section of Cardiology, VA Ann Arbor Healthcare System, MI (J.P.).
Nadia R SuttonFrom Department of Molecular and Integrative Physiology (A.E.B., D.J.P.) and Department of Internal Medicine (N.R.S., D.P.-D, H.L., J.R., Y.K., D.J.P.), Division of Cardiovascular Medicine University of Michigan Medical Center, Ann Arbor; and Section of Cardiology, VA Ann Arbor Healthcare System, MI (J.P.).
Danica Petrovic-DjergovicFrom Department of Molecular and Integrative Physiology (A.E.B., D.J.P.) and Department of Internal Medicine (N.R.S., D.P.-D, H.L., J.R., Y.K., D.J.P.), Division of Cardiovascular Medicine University of Michigan Medical Center, Ann Arbor; and Section of Cardiology, VA Ann Arbor Healthcare System, MI (J.P.).
Hui LiaoFrom Department of Molecular and Integrative Physiology (A.E.B., D.J.P.) and Department of Internal Medicine (N.R.S., D.P.-D, H.L., J.R., Y.K., D.J.P.), Division of Cardiovascular Medicine University of Michigan Medical Center, Ann Arbor; and Section of Cardiology, VA Ann Arbor Healthcare System, MI (J.P.).
Jessica J RayFrom Department of Molecular and Integrative Physiology (A.E.B., D.J.P.) and Department of Internal Medicine (N.R.S., D.P.-D, H.L., J.R., Y.K., D.J.P.), Division of Cardiovascular Medicine University of Michigan Medical Center, Ann Arbor; and Section of Cardiology, VA Ann Arbor Healthcare System, MI (J.P.).
Joan ParkFrom Department of Molecular and Integrative Physiology (A.E.B., D.J.P.) and Department of Internal Medicine (N.R.S., D.P.-D, H.L., J.R., Y.K., D.J.P.), Division of Cardiovascular Medicine University of Michigan Medical Center, Ann Arbor; and Section of Cardiology, VA Ann Arbor Healthcare System, MI (J.P.).
Yogendra KanthiFrom Department of Molecular and Integrative Physiology (A.E.B., D.J.P.) and Department of Internal Medicine (N.R.S., D.P.-D, H.L., J.R., Y.K., D.J.P.), Division of Cardiovascular Medicine University of Michigan Medical Center, Ann Arbor; and Section of Cardiology, VA Ann Arbor Healthcare System, MI (J.P.).
David J PinskyFrom Department of Molecular and Integrative Physiology (A.E.B., D.J.P.) and Department of Internal Medicine (N.R.S., D.P.-D, H.L., J.R., Y.K., D.J.P.), Division of Cardiovascular Medicine University of Michigan Medical Center, Ann Arbor; and Section of Cardiology, VA Ann Arbor Healthcare System, MI (J.P.). dpinsky@med.umich.edu.
VA Ann Arbor Healthcare System · US

Funding

TRAINING IN MOLECULAR AND CELLULAR CARDIOLOGYT32HL007853 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI David J. Pinsky · 1996 to 2026
$11.6M
SYTEMS AND INTEGRATIVE BIOLOGYT32GM008322 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LOW, MALCOLM JAMES · 1990 to 2020
$5.7M
K12: Career Development in Emergency Critical Care ResearchK12HL133304 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NEUMAR, ROBERT W., PINSKY, DAVID J. · 2016 to 2020
$2.2M
Vascular Ectonucleotidase Regulation of Ischemic StrokeR01NS087147 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PINSKY, DAVID J. · 2015 to 2019
$2.1M
Thrombo-Inflammatory Role of CD39 In Vascular StasisR01HL127151 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PINSKY, DAVID J. · 2015 to 2018
$2.0M
CD39 in Vein Graft ArterializationK08HL131993 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KANTHI, YOGENDRA · 2016 to 2020
$837k
NHLBI NIH HHS K08 HL131993NHLBI NIH HHS K12 HL133304NHLBI NIH HHS L30 HL129373NHLBI NIH HHS R01 HL127151NHLBI NIH HHS T32 HL007853NIGMS NIH HHS T32 GM008322NINDS NIH HHS R01 NS087147
6 · The paper itself

Abstract

backgroundCerebral tissue damage after an ischemic event can be exacerbated by inflammation and thrombosis. Elevated extracellular ATP and ADP levels are associated with cellular injury, inflammation, and thrombosis. Ectonucleoside triphosphate diphosphohydrolase-1 (CD39), an enzyme expressed on the plasmalemma of leukocytes and endothelial cells, suppresses platelet activation and leukocyte infiltration by phosphohydrolyzing ATP/ADP. To investigate the effects of increased CD39 in an in vivo cerebral ischemia model, we developed a transgenic mouse expressing human CD39 (hCD39).

methodsA floxed-stop sequence was inserted between the promoter and the hCD39 transcriptional start site, generating a mouse in which the expression of hCD39 can be controlled tissue-specifically using Cre recombinase mice. We generated mice that express hCD39 globally or in myeloid-lineage cells only. Cerebral ischemia was induced by middle cerebral artery occlusion. Infarct volumes were quantified by MRI after 48 hours.

resultsBoth global and transgenic hCD39- and myeloid lineage CD39-overexpressing mice (transgenic, n=9; myeloid lineage, n=6) demonstrated significantly smaller cerebral infarct volumes compared with wild-type mice. Leukocytes from ischemic and contralateral hemispheres were analyzed by flow cytometry. Although contralateral hemispheres had equal numbers of macrophages and neutrophils, ischemic hemispheres from transgenic mice had less infiltration (n=4). Transgenic mice showed less neurological deficit compared with wild-type mice (n=6).

conclusionsThis is the first report of transgenic overexpression of CD39 in mice imparting a protective phenotype after stroke, with reduced leukocyte infiltration, smaller infarct volumes, and decreased neurological deficit. CD39 overexpression, either globally or in myeloid lineage cells, quenches postischemic leukosequestration and reduces stroke-induced neurological injury.

Indexed as

AnimalsAntigens, CDApyraseBrain IschemiaCell LineageGene ExpressionHumansMaleMiceMice, Inbred C57BLMice, TransgenicMyeloid CellsTransgenesAntigens, CDApyraseCD39 antigenCD39inflammation

Identifiers

PMID28377485
PMCPMC5643044
OpenAlexW2604996749

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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.