Evidence map›Paper›PMID 26608888›Full record

ArticlePurinergic signalling2016

Adenosine A1 receptors contribute to immune regulation after neonatal hypoxic ischemic brain injury.

Max Winerdal, Malin E Winerdal, Ying-Qing Wang, Bertil B Fredholm, Ola Winqvist, Ulrika Ådén

Open access · bronzeAbstract read
In one paragraph

Article in Purinergic signalling, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
6.9field-weighted citation impact, top 4% 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

16 citing papers in PubMed, 36 citations in OpenAlex.

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  5. Targeting purine metabolism in ovarian cancer.Journal of ovarian research · 2022
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  6. Review
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  8. Review
  9. Theranostics · 2021
    Article
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  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Purinergic Signalling: Therapeutic Developments.Frontiers in pharmacology · 2017
    Review
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

6 authors at 2 institutions in 2 countries.

Max WinerdalDepartment of Women's and Children's Health, Karolinska Institutet, 17176, Stockholm, Sweden. max.winerdal@medsci.se.
Malin E WinerdalDepartment of Medicine, Karolinska Institutet, 17176, Stockholm, Sweden. malin.winerdal@ki.se.
Ying-Qing WangDepartment of Physiology and Pharmacology, Karolinska Institutet, 17176, Stockholm, Sweden. yqwang001@sina.com.
Bertil B FredholmDepartment of Physiology and Pharmacology, Karolinska Institutet, 17176, Stockholm, Sweden. bertil.fredholm@ki.se.
Ola WinqvistDepartment of Medicine, Karolinska Institutet, 17176, Stockholm, Sweden. ola.winqvist@karolinska.se.
Ulrika ÅdénDepartment of Women's and Children's Health, Karolinska Institutet, 17176, Stockholm, Sweden. ulrika.aden@ki.se.
Karolinska Institutet · SEShanghai Institute of Materia Medica · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neonatal brain hypoxic ischemia (HI) often results in long-term motor and cognitive impairments. Post-ischemic inflammation greatly effects outcome and adenosine receptor signaling modulates both HI and immune cell function. Here, we investigated the influence of adenosine A1 receptor deficiency (A1R(-/-)) on key immune cell populations in a neonatal brain HI model. Ten-day-old mice were subjected to HI. Functional outcome was assessed by open locomotion and beam walking test and infarction size evaluated. Flow cytometry was performed on brain-infiltrating cells, and semi-automated analysis of flow cytometric data was applied. A1R(-/-) mice displayed larger infarctions (+33%, p < 0.05) and performed worse in beam walking tests (44% more mistakes, p < 0.05) than wild-type (WT) mice. Myeloid cell activation after injury was enhanced in A1R(-/-) versus WT brains. Activated B lymphocytes expressing IL-10 infiltrated the brain after HI in WT, but were less activated and did not increase in relative frequency in A1R(-/-). Also, A1R(-/-) B lymphocytes expressed less IL-10 than their WT counterparts, the A1R antagonist DPCPX decreased IL-10 expression whereas the A1R agonist CPA increased it. CD4(+) T lymphocytes including FoxP3(+) T regulatory cells, were unaffected by genotype, whereas CD8(+) T lymphocyte responses were smaller in A1R(-/-) mice. Using PCA to characterize the immune profile, we could discriminate the A1R(-/-) and WT genotypes as well as sham operated from HI-subjected animals. We conclude that A1R signaling modulates IL-10 expression by immune cells, influences the activation of these cells in vivo, and affects outcome after HI.

Indexed as

Adenosine A1 Receptor AgonistsAdenosine A1 Receptor AntagonistsAnimalsAnimals, NewbornBrainBrain IschemiaCD4-Positive T-LymphocytesCerebral InfarctionFemaleHypoxia, BrainInterleukin-10MaleMiceMice, Inbred C57BLMice, KnockoutMotor ActivityAdenosine A1 Receptor AgonistsAdenosine A1 Receptor AntagonistsIL10 protein, mouseInterleukin-10Receptor, Adenosine A1Adenosine A1 receptorBrain hypoxic-ischemiaCellular immunityNeonatologyNeuroimmunomodulationStatistical data interpretation

Identifiers

PMID26608888
PMCPMC4749537
OpenAlexW2304863973

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.