Evidence map›Paper›PMID 23478188›Full record

Trial reportThe Journal of experimental medicine2013

Plasma glutamate-modulated interaction of A2AR and mGluR5 on BMDCs aggravates traumatic brain injury-induced acute lung injury.

Shuang-Shuang Dai, Hao Wang, Nan Yang, Jian-Hong An, Wei Li, Ya-Lei Ning, Pei-Fang Zhu, Jiang-Fan Chen, Yuan-Guo Zhou

Open access · bronzeAbstract readClinical Trial
In one paragraph

Trial report in The Journal of experimental medicine, 2013. 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
1.9field-weighted citation impact, top 15% 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, 48 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. A Novel Role of AFrontiers in pharmacology · 2021
    Article
  11. AJournal of cellular and molecular medicine · 2020
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Dexmedetomidine Protects Against Traumatic Brain Injury-Induced Acute Lung Injury in Mice.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  17. Article
  18. Review
  19. Innate immune responses to trauma.Nature immunology · 2018
    Review
  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

9 authors at 3 institutions in 2 countries.

Shuang-Shuang DaiDepartment of Biochemistry and Molecular Biology, State Key Laboratory of Trauma, Burn, and Combined Injury, Third Military Medical University, Chongqing 400042, China.
Hao Wang
Nan Yang
Jian-Hong An
Wei Li
Ya-Lei Ning
Pei-Fang Zhu
Jiang-Fan Chen
Yuan-Guo Zhou
Daping Hospital · CNArmy Medical University · CNBoston University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The bone marrow-derived cell (BMDC)-associated inflammatory response plays a key role in the development of acute lung injury (ALI). Activation of adenosine A2A receptor (A2AR) is generally considered to be antiinflammatory, inhibiting BMDC activities to protect against ALI. However, in the present study, we found that in a mouse model of neurogenic ALI induced by severe traumatic brain injury (TBI), BMDC A2AR exerted a proinflammatory effect, aggravating lung damage. This is in contrast to the antiinflammatory effect observed in the mouse oleic acid-induced ALI model (a nonneurogenic ALI model.) Moreover, the A2AR agonist CGS21680 aggravated, whereas the antagonist ZM241385 attenuated, the severe TBI-induced lung inflammatory damage in mice. Further investigation of white blood cells isolated from patients or mouse TBI models and of cultured human or mouse neutrophils demonstrated that elevated plasma glutamate after severe TBI induced interaction between A2AR and the metabotropic glutamate receptor 5 (mGluR5) to increase phospholipase C-protein kinase C signaling, which mediated the proinflammatory effect of A2AR. These results are in striking contrast to the well-known antiinflammatory and protective role of A2AR in nonneurogenic ALI and indicate different therapeutic strategies should be used for nonneurogenic and neurogenic ALI treatment when targeting A2AR.

Indexed as

Signal TransductionAcute Lung InjuryAdenosineAdenosine A2 Receptor AgonistsAdultAnimalsBone Marrow CellsBrain InjuriesDisease Models, AnimalFemaleGlutamic AcidHumansMaleMiceMice, KnockoutMiddle Aged2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosineAdenosineAdenosine A2 Receptor AgonistsGlutamic AcidGRM5 protein, humanGrm5 protein, mousePhenethylaminesProtein Kinase CReceptor, Adenosine A2AReceptor, Metabotropic Glutamate 5Receptors, Metabotropic GlutamateTriazinesTriazolesType C PhospholipasesZM 241385

Identifiers

PMID23478188
PMCPMC3620361
OpenAlexW2123992098

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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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.