Evidence map›Paper›PMID 28539655›Full record

ArticleScientific reports2017

Angiopoietin-1 enhances neutrophil chemotaxis in vitro and migration in vivo through interaction with CD18 and release of CCL4.

Amanda Burnett, Ingrid Gomez, David Davila De Leon, Mark Ariaans, Pavlos Progias, Richard A Kammerer, Guillermo Velasco, Marie Marron, Paul Hellewell, Victoria Ridger

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Targeting Neutrophil βBiomolecules · 2023
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
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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

10 authors at 5 institutions in 3 countries.

Amanda BurnettDepartment of Cardiovascular Science, Faculty of Medicine, Dentistry and Health. University of Sheffield, Sheffield, UK.
Ingrid GomezDepartment of Cardiovascular Science, Faculty of Medicine, Dentistry and Health. University of Sheffield, Sheffield, UK.
David Davila De LeonDepartment of Biochemistry and Molecular Biology, School of Biology, Complutense University, 28040, Madrid, Spain.
Mark AriaansDepartment of Cardiovascular Science, Faculty of Medicine, Dentistry and Health. University of Sheffield, Sheffield, UK.
Pavlos ProgiasWellcome Trust Centre for Cell-Matrix Research, Faculty of Life Sciences, University of Manchester, Manchester, M13 9PT, UK.
Richard A KammererLaboratory of Biomolecular Research, Division of Biology and Chemistry, Paul Scherrer Institut, CH-5232, Villigen PSI, Switzerland.
Guillermo VelascoDepartment of Biochemistry and Molecular Biology, School of Biology, Complutense University, 28040, Madrid, Spain.
Marie MarronDepartment of Cardiovascular Science, Faculty of Medicine, Dentistry and Health. University of Sheffield, Sheffield, UK.
Paul HellewellCollege of Health and Life Sciences, Brunel University London, Uxbridge, UB8 3PH, UK.ORCID 0000-0002-2044-1570
Victoria RidgerDepartment of Cardiovascular Science, Faculty of Medicine, Dentistry and Health. University of Sheffield, Sheffield, UK. V.C.Ridger@Sheffield.ac.uk.ORCID 0000-0003-4163-669X
University of Sheffield · GBUniversidad Complutense de Madrid · ESBrunel University of London · GBPaul Scherrer Institute · CHWellcome Centre for Cell-Matrix Research · GB

Funding

British Heart Foundation FS/06/081/21722British Heart Foundation PG/14/38/30862
6 · The paper itself

Abstract

Angiopoietins are a family of growth factors that are ligands for the tyrosine kinase receptor, Tie2. Angiopoietin 1 (Ang-1) is agonistic for Tie2, plays a key role in blood vessel maturation and stability and has been shown to possess anti-inflammatory properties. However, Tie2 expression has been demonstrated on human neutrophils and the observation that neutrophils migrate in response to Ang-1 in vitro has confounded research into its exact role in inflammation as well as its potential use as a therapeutic agent. We used a mouse model of peritoneal neutrophilic inflammation to determine if Ang-1 could stimulate neutrophil migration in vivo. Tie2 expression was demonstrated on mouse neutrophils. In addition, recombinant human Ang-1 induced significant chemotaxis of isolated mouse neutrophils in a Tie2- and CD18-dependent manner. Subsequently, co-immunoprecipitation of Ang-1 and CD18 demonstrated their interaction. Intraperitoneal injection of an engineered angiopoietin-1, MAT.Ang-1, induced significant neutrophil migration into the peritoneum and a significant increase in the levels of CCL4 in peritoneal lavage fluid. Depletion of resident peritoneal macrophages prior to, or concomitant injections of an anti-CCL4 antibody with MAT.Ang-1 resulted in a significant reduction in neutrophil recruitment. These data indicate a pro-inflammatory role for Ang-1 with respect to neutrophil recruitment.

Indexed as

Angiopoietin-1AnimalsCD18 AntigensCell MovementChemokine CCL4ChemotaxisDisease Models, AnimalGene Expression RegulationHumansInflammationMiceNeutrophilsPeritoneal LavagePeritoneumReceptor, TIE-2Recombinant ProteinsAngiopoietin-1Angpt1 protein, mouseCD18 AntigensChemokine CCL4Receptor, TIE-2Recombinant ProteinsTek protein, mouse

Identifiers

PMID28539655
PMCPMC5443761
OpenAlexW2612639294

What OpenQuestion holds

Textmetadata
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.