Evidence map›Paper›PMID 19095957›Full record

ArticleThe American journal of pathology2009

Functional and ultrastructural analysis of annexin A1 and its receptor in extravasating neutrophils during acute inflammation.

Thaís Santana Gastardelo, Amílcar Sabino Damazo, Jesmond Dalli, Roderick J Flower, Mauro Perretti, Sonia Maria Oliani

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2009. 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
1.8field-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, 74 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Annexin A1 Mimetic Peptide AcFrontiers in immunology · 2021
    Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Annexin A1 mediates hydrogen sulfide properties in the control of inflammation.The Journal of pharmacology and experimental therapeutics · 2014
    Article
  17. Article
  18. Review
  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

6 authors at 4 institutions in 2 countries.

Thaís Santana GastardeloPost-Graduation in Morphology, Federal University of São Paulo, Paulista School of Medicine (EPM), São Paulo, Brazil.
Amílcar Sabino Damazo
Jesmond Dalli
Roderick J Flower
Mauro Perretti
Sonia Maria Oliani
Queen Mary University of London · GBUniversidade Estadual de Goiás · BRUniversidade Estadual Paulista (Unesp) · BRUniversidade Federal de São Paulo · BR

Funding

Wellcome TrustWellcome Trust 069234/Z/02/Z
6 · The paper itself

Abstract

The purpose of this study was twofold: to reveal cellular events associated with the protective role of endogenous annexin A1 (AnxA1) in inflammation and to highlight the potential involvement of members of the formyl peptide receptor (Fpr) family in this process. We found that wild-type, AnxA1-null, and Fpr1-null mice all displayed an intense neutrophil recruitment into the peritoneal cavity as assessed 4 hours after carrageenin injection, and that this recruitment was most pronounced in AnxA1-null mice. In addition, this cell influx could be inhibited by the AnxA1 pharmacophore peptide, Ac2-26, in wild-type, AnxA1-null, and Fpr1-null mice, but was restored when co-treated with the pan-receptor antagonist Boc2. Using the LacZ gene reporter assay, an enhancement of AnxA1 gene promoter activity in extravasated neutrophils was evident in AnxA1-null mice; again this response was reduced after peptide treatment. The lack of functional involvement of Fpr1 prompted us to monitor the structurally related receptor Fpr2. We report, for the first time, the ultrastructural immunocytochemical co-localization of Fpr2 with AnxA1 in neutrophils that migrate into the mesenteric microcirculation and extravasate into the peritoneal fluid. Collectively, these data provide in vivo support to the hypothesis that endogenous AnxA1 is an essential effector of endogenous anti-inflammation and provide an ultrastructural indication that this mediator interacts with Fpr2 in murine neutrophils. We believe that these findings could significantly affect the development of novel therapeutics, which are modeled after the anti-migratory actions of AnxA1.

Indexed as

AnimalsAnnexin A1Chemotaxis, LeukocyteGene ExpressionImmunohistochemistryInflammationMaleMiceMice, Mutant StrainsNeutrophilsReceptors, Formyl PeptideReverse Transcriptase Polymerase Chain ReactionAnnexin A1formyl peptide receptor 2, mouseFpr1 protein, mouseReceptors, Formyl Peptide

Identifiers

PMID19095957
PMCPMC2631330
OpenAlexW2118759665

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.