Evidence map›Paper›PMID 10704090›Full record

ArticleMediators of inflammation1999

Differential modulation of annexin I binding sites on monocytes and neutrophils.

H S Euzger, R J Flower, N J Goulding, M Perretti

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

11 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Unconventional secretion of annexins and galectins.Seminars in cell & developmental biology · 2018
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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

4 authors at 1 institution in 1 country.

H S EuzgerDepartment of Biochemical Pharmacology, The William Harvey Research Institute, London, UK.
R J Flower
N J Goulding
M Perretti
William Harvey Research Institute · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

Specific binding sites for the anti-inflammatory protein annexin I have been detected on the surface of human monocytes and polymorphonuclear leukocytes (PMN). These binding sites are proteinaceous in nature and are sensitive to cleavage by the proteolytic enzymes trypsin, collagenase, elastase and cathepsin G. When monocytes and PMN were isolated independently from peripheral blood, only the monocytes exhibited constitutive annexin I binding. However PMN acquired the capacity to bind annexin I following co-culture with monocytes. PMN incubation with sodium azide, but not protease inhibitors, partially blocked this process. A similar increase in annexin I binding capacity was also detected in PMN following adhesion to endothelial monolayers. We propose that a juxtacrine activation rather than a cleavage-mediated transfer is involved in this process. Removal of annexin I binding sites from monocytes with elastase rendered monocytes functionally insensitive to full length annexin I or to the annexin I-derived pharmacophore, peptide Ac2-26, assessed as suppression of the respiratory burst. These data indicate that the annexin I binding site on phagocytic cells may have an important function in the feedback control of the inflammatory response and their loss through cleavage could potentiate such responses.

Indexed as

Respiratory BurstAmino Acid SequenceAnnexin A1Anti-Inflammatory Agents, Non-SteroidalBinding SitesEndopeptidasesFlow CytometryGlycineHumansIn Vitro TechniquesMolecular Sequence DataMonocytesNeutrophilsPeptide FragmentsPeptidesSerine Proteinase InhibitorsAnnexin A1annexin A1 peptide (2-26)Anti-Inflammatory Agents, Non-SteroidalEndopeptidasesGlycinePeptide FragmentsPeptidesSerine Proteinase InhibitorssivelestatSulfonamides

Identifiers

PMID10704090
PMCPMC1781781
OpenAlexW2116459589

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.