Evidence map›Paper›PMID 23202369›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2013

Neutrophil proteinase 3 acts on protease-activated receptor-2 to enhance vascular endothelial cell barrier function.

Christopher J Kuckleburg, Peter J Newman

Abstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

25 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
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  9. Article
  10. MeningiticFrontiers in cellular neuroscience · 2022
    Article
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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

2 authors at 1 institution in 1 country.

Christopher J KuckleburgBlood Research Institute, BloodCenter of Wisconsin, 8727 Watertown Plank Rd, Milwaukee, WI 53051, USA. christopher.kuckleburg@bcw.edu
Peter J Newman
Versiti Blood Center of Wisconsin · US

Funding

MOLECULAR BIOLOGY &FUNCTION OF PLATELET MEMBRANE GP130R01HL040926 · NHLBI · VERSITI WISCONSIN, INC. · PI NEWMAN, PETER J · 1988 to 2017
$7.4M
RESEARCH TRAINING IN TRANSFUSION SCIENCET32HL007209 · NHLBI · VERSITI WISCONSIN, INC. · PI WHITE, II, GILBERT C. · 1985 to 2019
$2.9M
NHLBI NIH HHS HL-07209NHLBI NIH HHS HL40926NHLBI NIH HHS R01 HL040926NHLBI NIH HHS T32 HL007209
6 · The paper itself

Abstract

objectiveThe principle role of the vascular endothelium is to present a semi-impermeable barrier to soluble factors and circulating cells, while still permitting the passage of leukocytes from the bloodstream into the tissue. The process of diapedesis involves the selective disruption of endothelial cell junctions, which could compromise vascular integrity. It is therefore somewhat surprising that neutrophil transmigration does not significantly impair endothelial barrier function. We examined whether neutrophils might secrete factors that promote vascular integrity during the latter stages of neutrophil transmigration, in particular, the role of neutrophil serine proteinase 3 (PR3). METHODS AND

resultsEndothelial cells were treated with PR3 either in its soluble form or in a complex form with cell surface NB1. We observed that PR3 mediated the enhancement of endothelial cell junctional integrity and that this required its proteolytic activity, as well as endothelial cell expression of the protease-activated receptor-2. Importantly, PR3 suppressed the vascular permeability changes and disruption of junctional proteins induced by the action of protease-activated receptor-1 agonists.

conclusionsThese findings establish the potential for neutrophil-derived PR3 to play a role in reestablishing vascular integrity after leukocyte transmigration and in protecting endothelial cells from protease-activated receptor-1-induced permeability changes that occur during thrombotic and inflammatory events.

Indexed as

Capillary PermeabilityTransendothelial and Transepithelial MigrationCalcium SignalingCoculture TechniquesGPI-Linked ProteinsHEK293 CellsHumansHuman Umbilical Vein Endothelial CellsIsoantigensMyeloblastinNeutrophilsrac1 GTP-Binding ProteinReceptor, PAR-1Receptor, PAR-2Receptors, Cell SurfaceRNA InterferenceCD177 protein, humanGPI-Linked ProteinsIsoantigensMyeloblastinrac1 GTP-Binding ProteinRAC1 protein, humanReceptor, PAR-1Receptor, PAR-2Receptors, Cell Surface

Identifiers

PMID23202369
PMCPMC3562705
OpenAlexW2123158490

What OpenQuestion holds

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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.