Evidence map›Paper›PMID 26803520›Full record

ArticleInternational immunopharmacology2016

The role of the Annexin-A1/FPR2 system in the regulation of mast cell degranulation provoked by compound 48/80 and in the inhibitory action of nedocromil.

Ajantha Sinniah, Samia Yazid, M Perretti, Egle Solito, R J Flower

Open access · hybridAbstract read
In one paragraph

Article in International immunopharmacology, 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
2.3field-weighted citation impact, top 12% 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, 27 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Annexin Animal Models-From Fundamental Principles to Translational Research.International journal of molecular sciences · 2021
    Review
  7. Annexin A1 Mimetic Peptide AcFrontiers in immunology · 2021
    Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. 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

5 authors at 2 institutions in 1 country.

Ajantha SinniahCentre for Biochemical Pharmacology, William Harvey Research Institute, St Barts and the Royal London School of Medicine, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.
Samia YazidMolecular Therapy Department, Institute of Ophthalmology, 11/14 Bath Street, London EC1V 9EL, UK.
M PerrettiCentre for Biochemical Pharmacology, William Harvey Research Institute, St Barts and the Royal London School of Medicine, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.
Egle SolitoCentre for Translational Medicine and Therapeutics, William Harvey Research Institute, St Barts and the Royal London School of Medicine, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.
R J FlowerCentre for Biochemical Pharmacology, William Harvey Research Institute, St Barts and the Royal London School of Medicine, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK. Electronic address: r.j.flower@qmul.ac.uk.
Queen Mary University of London · GBWilliam Harvey Research Institute · GB

Funding

Wellcome Trust 085903
6 · The paper itself

Abstract

1.We investigated the role of Annexin (ANX)-A1 and its receptor, ALX/FPR2, in the regulation of mast cell degranulation produced by compound 48/80. 2.Both human cord-blood derived mast cells (CBDMCs) and murine bone marrow derived mast cells (BMDMCs) release phosphorylated ANX-A1 during treatment with glucocorticoids or the mast cell 'stabilising' drugs ketotifen and nedocromil. 3.Compound 48/80 also stimulated ANX-A1 phosphorylation and release and this was also potentiated by nedocromil. Anti-ANX-A1 neutralising monoclonal antibodies (Mabs) enhanced the release of pro-inflammatory mediators in response to compound 48/80. 4.Nedocromil and ketotifen potently inhibited the release of histamine, PGD2, tryptase and β-hexosaminidase from mast cells challenged with compound 48/80. Anti-ANX-A1 neutralising Mabs prevented the inhibitory effect of these drugs. 5.BMDMCs derived from Anx-A1−/− mice were insensitive to the inhibitory effects of nedocromil or ketotifen but cells retained their sensitivity to the inhibitory action of hu-r-ANX-A1. 6.The fpr2/3 antagonist WRW4 blocked the action of nedocromil on PGD2, but not histamine, release. BMDMCs derived from fpr2/3−/− mice were insensitive to the inhibitory effects of nedocromil on PGD2, but not histamine release. 7.Compound 48/80 stimulated both p38 and JNK phosphorylation in CBDMCs and this was inhibited by nedocromil. Inhibition of p38 phosphorylation was ANX-A1 dependent. 8.We conclude that ANX-A1 is an important regulator of mast cell reactivity to compound 48/80 exerting a negative feedback effect through a mechanism that depends at least partly on the FPR receptor.

Indexed as

AnimalsAnnexin A1Anti-Allergic AgentsAnti-Inflammatory AgentsBone Marrow CellsCell DegranulationDexamethasoneFetal BloodHumansIndolesKetotifenMaleimidesMAP Kinase Kinase 4Mast CellsMice, Inbred BALB CMice, Inbred C57BL2-(1-(3-dimethylaminopropyl)-5-methoxyindol-3-yl)-3-(1H-indol-3-yl)maleimideAnnexin A1Anti-Allergic AgentsAnti-Inflammatory AgentsDexamethasoneformyl peptide receptor 2, mouseFPR2 protein, humanIndolesKetotifenMaleimidesMAP Kinase Kinase 4Nedocromilp38 Mitogen-Activated Protein Kinasesp-Methoxy-N-methylphenethylamineProtein Kinase CProtein Kinase InhibitorsReceptors, Formyl PeptideReceptors, LipoxinANX-A1Compound 48/80CromonesMast cellPKCPP2A

Identifiers

PMID26803520
PMCPMC4760273
OpenAlexW2286752136

What OpenQuestion holds

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LicenceCC BY
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.