Evidence map›Paper›PMID 20132822›Full record

ArticleJournal of molecular and cellular cardiology2010

A(3) adenosine receptor activation during reperfusion reduces infarct size through actions on bone marrow-derived cells.

Zhi-Dong Ge, Dharini van der Hoeven, Jason E Maas, Tina C Wan, John A Auchampach

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

30 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Review
  3. Adenosine AInternational journal of molecular sciences · 2024
    Review
  4. Extrahelical Binding Site for a 1Molecular pharmacology · 2024
    Article
  5. Article
  6. Species dependence of APurinergic signalling · 2023
    Review
  7. Article
  8. Characterization of Dual-Acting AACS pharmacology & translational science · 2022
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Purinergic Regulation of Neutrophil Function.Frontiers in immunology · 2018
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

Zhi-Dong GeDepartment of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Dharini van der Hoeven
Jason E Maas
Tina C Wan
John A Auchampach
Medical College of Wisconsin · US

Funding

Role of Adenosine Receptors in Tissue ProtectionR01HL077707 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI AUCHAMPACH, JOHN A · 2005 to 2014
$3.4M
NHLBI NIH HHS R01 HL077707
6 · The paper itself

Abstract

The goal of this study was to examine whether the A(3) adenosine receptor (A(3)AR) agonist Cl-IB-MECA protects against myocardial ischemia/reperfusion injury when administered at the time of reperfusion in an in vivo mouse model of infarction induced by 30min of coronary occlusion and 24h of reperfusion. Treating B6 wild-type with Cl-IB-MECA during the reperfusion phase (100microg/kg i.v. bolus+0.3microg/kg/min subcutaneously via implantation of Alzet mini-osmotic pumps) reduced myocardial infarct size approximately 37% from 50.1+/-2.5% in vehicle-treated mice to 31.6+/-2.8% in Cl-IB-MECA-treated mice, and significantly reduced the number of leukocytes that infiltrated into the ischemic-reperfused myocardium. Cl-IB-MECA did not reduce infarct size or limit leukocyte accumulation in studies using B6 congenic A(3)AR gene "knock-out" mice or in chimeric mice lacking the expression of A(3)ARs in bone marrow (BM)-derived cells. Subsequent mechanistic studies demonstrated that Cl-IB-MECA inhibited migration of mouse neutrophils isolated from BM towards the chemotactic substance c5a in trans-well migration assays, and inhibited leukocyte migration into the peritoneal cavity in a mouse model of thioglycollate-induced peritonitis. We conclude that treating with the A(3)AR agonist Cl-IB-MECA at the time of reperfusion provides effective protection from ischemia/reperfusion injury in the heart through activation of the A(3)AR expressed in BM-derived cells, potentially by suppressing the robust inflammatory reaction that occurs during reperfusion and neutrophil-mediated tissue injury.

Indexed as

AdenosineAdenosine A3 Receptor AgonistsAnimalsBlood PressureBone Marrow CellsBone Marrow TransplantationCell MovementHistamineMaleMiceMice, Inbred C57BLMice, KnockoutMyocardial InfarctionMyocardial Reperfusion InjuryNeutrophilsReceptor, Adenosine A32-chloro-N(6)-(3-iodobenzyl)adenosine-5'-N-methyluronamideAdenosineAdenosine A3 Receptor AgonistsHistamineReceptor, Adenosine A3

Identifiers

PMID20132822
PMCPMC2885516
OpenAlexW2067846325

What OpenQuestion holds

Textmetadata
LicenceTDM
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.