Evidence map›Paper›PMID 27338585›Full record

ArticleArthritis research & therapy2016

Endothelial progenitor cells are differentially impaired in ANCA-associated vasculitis compared to healthy controls.

B Wilde, A Mertens, S J Arends, R P Rouhl, R Bijleveld, J Huitema, S A Timmermans, J Damoiseaux, O Witzke, A M Duijvestijn and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Arthritis research & therapy, 2016. 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
1.0field-weighted citation impact, top 21% 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, 14 citations in OpenAlex.

  1. Review
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  8. Frontiers in bioengineering and biotechnology · 2020
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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

13 authors at 3 institutions in 2 countries.

B WildeImmunology, Maastricht University, PO Box 5800, 6202 AZ, Maastricht, The Netherlands.
A MertensImmunology, Maastricht University, PO Box 5800, 6202 AZ, Maastricht, The Netherlands.
S J ArendsImmunology, Maastricht University, PO Box 5800, 6202 AZ, Maastricht, The Netherlands.
R P RouhlImmunology, Maastricht University, PO Box 5800, 6202 AZ, Maastricht, The Netherlands.
R BijleveldImmunology, Maastricht University, PO Box 5800, 6202 AZ, Maastricht, The Netherlands.
J HuitemaImmunology, Maastricht University, PO Box 5800, 6202 AZ, Maastricht, The Netherlands.
S A TimmermansImmunology, Maastricht University, PO Box 5800, 6202 AZ, Maastricht, The Netherlands.
J DamoiseauxCentral Diagnostic Laboratory, Maastricht University Medical Center, Maastricht, The Netherlands.
O WitzkeDepartment of Nephrology, University Duisburg-Essen, University Hospital Essen, Essen, Germany.
A M DuijvestijnImmunology, Maastricht University, PO Box 5800, 6202 AZ, Maastricht, The Netherlands.
P van PaassenImmunology, Maastricht University, PO Box 5800, 6202 AZ, Maastricht, The Netherlands.
R J van OostenbruggeDepartment of Neurology, University Hospital Maastricht, Maastricht, The Netherlands.
J W Cohen TervaertImmunology, Maastricht University, PO Box 5800, 6202 AZ, Maastricht, The Netherlands. jw.cohentervaert@maastrichtuniversity.nl.
Maastricht University · NLMaastricht University Medical Centre · NLUniversity of Duisburg-Essen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEndothelial progenitor cells (EPC) are of major importance in vascular repair under healthy circumstances. Vascular injury in need of repair occurs frequently in ANCA-associated vasculitis (AAV). A specialized T cell subset enhancing EPC function and differentiation has recently been described. These angiogenic T cells (Tang) may have an important impact on the vascular repair process. Therefore, the aim of our study was to investigate EPC and Tang in AAV.

methodsFifty-three patients suffering from AAV and 29 healthy controls (HC) were enrolled in our study. Forty-four patients were in remission, nine patients were in active state of disease. Patients were either untreated or were under monotherapy with low-dose steroids (max. 5 mg/day) at the time of sampling. Circulating EPC and Tang were determined by flow cytometry (FACS). The functional capacity of EPC was assessed by established cell culture methods.

resultsCirculating EPC were significantly decreased in AAV as compared to HC. The capacity of EPC to differentiate and proliferate was differentially impaired in patients as compared to HC. The outgrowth of endothelial colony-forming cells (ECFC) was severely decreased in patients whereas colony-forming units-endothelial cell (CFU-EC) outgrowth was unaffected. ECFC and CFU-EC differentiation was strictly T cell-dependent. Patients with a relapsing disease course had an impaired ECFC outgrowth and expansion of Tang as compared to patients with a stable, nonrelapsing disease.

conclusionsThe differentiation process of EPC is impaired in AAV. This may favor insufficient vascular repair promoting a relapsing disease course. Finally, these factors may explain a higher cardiovascular morbidity as has been previously documented in AAV.

Indexed as

AdultAgedAnti-Neutrophil Cytoplasmic Antibody-Associated VasculitisCell DifferentiationCell ProliferationEndothelial Progenitor CellsFemaleFlow CytometryHumansMaleMiddle AgedT-Lymphocyte SubsetsAutoantibodiesEndothelial progenitor cellsVasculitis

Identifiers

PMID27338585
PMCPMC4918016
OpenAlexW2471652037

What OpenQuestion holds

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Registered trials

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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.