Evidence map›Paper›PMID 31369589›Full record

Observational studyPloS one2019

Emergence of AnnexinVpos CD31neg CD42blow/neg extracellular vesicles in plasma of humans at extreme altitude.

Olaf Utermöhlen, Kristin Jakobshagen, Birgit Blissenbach, Katja Wiegmann, Tobias Merz, Jacqueline Pichler Hefti, Martin Krönke

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

Observational study in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 24% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
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

7 authors at 4 institutions in 3 countries.

Olaf UtermöhlenInstitute for Medical Microbiology, Immunology and Hygiene, University Hospital Cologne, Cologne, Germany.
Kristin JakobshagenInstitute for Medical Microbiology, Immunology and Hygiene, University Hospital Cologne, Cologne, Germany.
Birgit BlissenbachInstitute for Medical Microbiology, Immunology and Hygiene, University Hospital Cologne, Cologne, Germany.
Katja WiegmannInstitute for Medical Microbiology, Immunology and Hygiene, University Hospital Cologne, Cologne, Germany.
Tobias MerzDepartment of Intensive Care Medicine, University Hospital and University of Bern, Bern, Switzerland.
Jacqueline Pichler HeftiDepartment of Intensive Care Medicine, University Hospital and University of Bern, Bern, Switzerland.
Martin KrönkeInstitute for Medical Microbiology, Immunology and Hygiene, University Hospital Cologne, Cologne, Germany.
University Hospital Cologne · DEUniversity of Cologne · DEUniversity Hospital of Bern · CHUniversity of Bern · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHypobaric hypoxia has been reported to cause endothelial cell and platelet dysfunction implicated in the formation of microvascular lesions, and in its extremes may contribute to vascular leakage in high altitude pulmonary edema or blood brain barrier disruption leading to cerebral micro-hemorrhage (MH). Platelet function in the development of microvascular lesions remained ill defined, and is still incompletely understood. In this study platelet- and endothelial cell-derived extracellular vesicles (PEV and EEV, respectively) and cell adhesion molecules were characterized in plasma samples of members of a high altitude expedition to delineate the contribution of platelets and endothelial cells to hypobaric hypoxia-induced vascular dysfunction. METHODS AND

findingsIn this observational study, platelet and endothelial cell-derived extracellular vesicles were analysed by flow-cytometry in plasma samples from 39 mountaineers participating in a medical research climbing expedition to Himlung Himal, Nepal, 7,050m asl. Megakaryocyte/platelet-derived AnnexinVpos, PECAM-1 (CD31) and glycoprotein-1b (GP1b, CD42b) positive extracellular vesicles (PEV) constituted the predominant fraction of EV in plasma samples up to 6,050m asl. Exposure to an altitude of 7,050m led to a marked decline of CD31pos CD42neg EEV as well as of CD31pos CD42bpos PEV at the same time giving rise to a quantitatively prevailing CD31neg CD42blow/neg subpopulation of AnnexinVpos EV. An almost hundredfold increase in the numbers of this previously unrecognized population of CD31neg CD42blow/neg EV was observed in all participants reaching 7,050m asl.

conclusionsThe emergence of CD31neg CD42blow/neg EV was observed in all participants and thus represents an early hypoxic marker at extreme altitude. Since CD31 and CD42b are required for platelet-endothelial cell interactions, these hypobaric hypoxia-dependent quantitative and phenotypic changes of AnnexinVpos EV subpopulations may serve as early and sensitive indicators of compromised vascular homeostasis.

Indexed as

AltitudeAcclimatizationAnnexin A5Endothelial CellsExtracellular VesiclesHumansHypoxiaMiddle AgedPlatelet Endothelial Cell Adhesion Molecule-1Annexin A5ANXA5 protein, humanPECAM1 protein, humanPlatelet Endothelial Cell Adhesion Molecule-1

Identifiers

PMID31369589
PMCPMC6675110
OpenAlexW2964400122

What OpenQuestion holds

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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.