Evidence map›Paper›PMID 26786759›Full record

ArticleJournal of biomedical science2016

Endothelium-derived microparticles from chronically thromboembolic pulmonary hypertensive patients facilitate endothelial angiogenesis.

Daria Belik, Hilda Tsang, John Wharton, Luke Howard, Carmelo Bernabeu, Beata Wojciak-Stothard

Open access · diamondAbstract read
In one paragraph

Article in Journal of biomedical science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
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  6. Exosomes as Intercellular Messengers in Hypertension.International journal of molecular sciences · 2021
    Review
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  11. Article
  12. Article
  13. Endothelial microvesicles in hypoxic hypoxia diseases.Journal of cellular and molecular medicine · 2018
    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

6 authors at 3 institutions in 2 countries.

Daria BelikCentre for Pharmacology and Therapeutics, Department of Medicine, Imperial College London, London, UK.
Hilda TsangCentre for Pharmacology and Therapeutics, Department of Medicine, Imperial College London, London, UK.
John WhartonCentre for Pharmacology and Therapeutics, Department of Medicine, Imperial College London, London, UK.
Luke HowardNational Pulmonary Hypertension Service, Imperial College Healthcare NHS Trust, London, UK.
Carmelo BernabeuCentro de Investigaciones Biológicas, Consejo Superior de Investigaciones Científicas (CSIC), and Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), 28040, Madrid, Spain.
Beata Wojciak-StothardCentre for Pharmacology and Therapeutics, Department of Medicine, Imperial College London, London, UK. b.wojciak-stothard@imperial.ac.uk.
Imperial College London · GBConsejo Superior de Investigaciones Científicas · ESImperial College Healthcare NHS Trust · GB

Funding

British Heart Foundation PG 11/13/28765British Heart Foundation PG/12/67/29773Wellcome Trust
6 · The paper itself

Abstract

backgroundIncreased circulating levels of endoglin(+) endothelial microparticles (EMPs) have been identified in several cardiovascular disorders, related to severity. Endoglin is an auxilary receptor for transforming growth factor β (TGF-β) important in the regulation of vascular structure.

resultsWe quantified the number of microparticles in plasma of six patients with chronic thromboembolic pulmonary hypertension (CTEPH) and age- and sex-matched pulmonary embolic (PE) and healthy controls and investigated the role of microparticle endoglin in the regulation of pulmonary endothelial function in vitro. Results show significantly increased levels of endoglin(+) EMPs in CTEPH plasma, compared to healthy and disease controls. Co-culture of human pulmonary endothelial cells with CTEPH microparticles increased intracellular levels of endoglin and enhanced TGF-β-induced angiogenesis and Smad1,5,8 phosphorylation in cells, without affecting BMPRII expression. In an in vitro model, we generated endothelium-derived MPs with enforced membrane localization of endoglin. Co-culture of these MPs with endothelial cells increased cellular endoglin content, improved cell survival and stimulated angiogenesis in a manner similar to the effects induced by overexpressed protein.

conclusionsIncreased generation of endoglin(+) EMPs in CTEPH is likely to represent a protective mechanism supporting endothelial cell survival and angiogenesis, set to counteract the effects of vascular occlusion and endothelial damage.

Indexed as

AdultAgedAged, 80 and overCell-Derived MicroparticlesEndothelium, VascularFemaleHumansHypertension, PulmonaryMaleMiddle AgedNeovascularization, PathologicPulmonary Embolism

Identifiers

PMID26786759
PMCPMC4717540
OpenAlexW2282910760

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.