Evidence map›Paper›PMID 21854743›Full record

ArticleThe American journal of pathology2011

A3 adenosine receptor agonist reduces brain ischemic injury and inhibits inflammatory cell migration in rats.

In-Young Choi, Jae-Chul Lee, Chung Ju, Sunyoung Hwang, Geum-Sil Cho, Hyuk Woo Lee, Won Jun Choi, Lak Shin Jeong, Won-Ki Kim

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

46 citing papers in PubMed, 80 citations in OpenAlex.

  1. 4'-Thionucleosides as adenosine AMedicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026
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  9. Adenosine and adenosine receptors in metabolic imbalance-related neurological issues.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2024
    Review
  10. Article
  11. Role of Microglia in Stroke.Advances in neurobiology · 2024
    Review
  12. Microglia at the blood brain barrier in health and disease.Frontiers in cellular neuroscience · 2024
    Review
  13. First Potent Macrocyclic AACS pharmacology & translational science · 2023
    Article
  14. Species dependence of APurinergic signalling · 2023
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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

9 authors at 5 institutions in 3 countries.

In-Young ChoiDepartment of Neuroscience, College of Medicine, Korea University, Seoul, Republic of Korea.
Jae-Chul Lee
Chung Ju
Sunyoung Hwang
Geum-Sil Cho
Hyuk Woo Lee
Won Jun Choi
Lak Shin Jeong
Won-Ki Kim
Korea University · KREwha Womans University · KRNew Generation University College · ETDongguk University · KRSeoul National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A3 adenosine receptor (A3AR) is recognized as a novel therapeutic target for ischemic injury; however, the mechanism underlying anti-ischemic protection by the A3AR agonist remains unclear. Here, we report that 2-chloro-N(6)-(3-iodobenzyl)-5'-N-methylcarbamoyl-4'-thioadenosine (LJ529), a selective A3AR agonist, reduces inflammatory responses that may contribute to ischemic cerebral injury. Postischemic treatment with LJ529 markedly reduced cerebral ischemic injury caused by 1.5-hour middle cerebral artery occlusion, followed by 24-hour reperfusion in rats. This effect was abolished by the simultaneous administration of the A3AR antagonist MRS1523, but not the A2AAR antagonist SCH58261. LJ529 prevented the infiltration/migration of microglia and monocytes occurring after middle cerebral artery occlusion and reperfusion, and also after injection of lipopolysaccharides into the corpus callosum. The reduced migration of microglia by LJ529 could be related with direct inhibition of chemotaxis and down-regulation of spatiotemporal expression of Rho GTPases (including Rac, Cdc42, and Rho), rather than by biologically relevant inhibition of inflammatory cytokine/chemokine release (eg, IL-1β, TNF-α, and MCP-1) or by direct inhibition of excitotoxicity/oxidative stress (not affected by LJ529). The present findings indicate that postischemic activation of A3AR and the resultant reduction of inflammatory response should provide a promising therapeutic strategy for the treatment of ischemic stroke.

Indexed as

AdenosineAdenosine A3 Receptor AgonistsAnimalsBrain InfarctionBrain InjuriesBrain IschemiaCell MovementChemokine CCL2GlucoseInflammationInterleukin-1betaLipopolysaccharidesMaleMicrogliaMonocytesN-Methylaspartate2-chloro-N(6)-(3-iodobenzyl)-5'-N-methylcarbamoyl-4'-thioadenosineAdenosineAdenosine A3 Receptor AgonistsCcl2 protein, ratChemokine CCL2GlucoseInterleukin-1betaLipopolysaccharidesN-MethylaspartateReactive Oxygen Speciesrho GTP-Binding ProteinsThionucleosidesTumor Necrosis Factor-alpha

Identifiers

PMID21854743
PMCPMC3181366
OpenAlexW2139589500

What OpenQuestion holds

Textmetadata
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.