Evidence map›Paper›PMID 30367147›Full record

ArticleScientific reports2018

Endothelial cells release cardioprotective exosomes that may contribute to ischaemic preconditioning.

Sean M Davidson, Jaime A Riquelme, Ying Zheng, Jose M Vicencio, Sergio Lavandero, Derek M Yellon

Abstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
–field-weighted citation impact
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

72 citing papers in PubMed.

  1. Trial
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  18. Biological resilience in health and disease.Disease models & mechanisms · 2024
    Review
  19. Review
  20. Neuroadaptive Biochemical Mechanisms of Remote Ischemic Conditioning.International journal of molecular sciences · 2023
    Review

12 more citing papers are in PubMed but not listed here.

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.

Sean M DavidsonThe Hatter Cardiovascular Institute, University College London, London, United Kingdom. s.davidson@ucl.ac.uk.ORCID http://orcid.org/0000-0001-5182-4980
Jaime A RiquelmeThe Hatter Cardiovascular Institute, University College London, London, United Kingdom.
Ying ZhengThe Hatter Cardiovascular Institute, University College London, London, United Kingdom.
Jose M VicencioThe Hatter Cardiovascular Institute, University College London, London, United Kingdom.
Sergio LavanderoAdvanced Center for Chronic Diseases, Facultad de Ciencias Químicas y Farmacéuticas, Universidad de Chile, 8380494, Santiago, Chile.ORCID http://orcid.org/0000-0003-4258-1483
Derek M YellonThe Hatter Cardiovascular Institute, University College London, London, United Kingdom.

Funding

Medical Research Council MR/K002066/1
6 · The paper itself

Abstract

Extracellular vesicles (EVs) such as exosomes are nano-sized vesicles that carry proteins and miRNAs and can transmit signals between cells. We hypothesized that exosomes from endothelial cells can transmit protective signals to cardiomyocytes. Co-culture of primary adult rat cardiomyocytes with normoxic HUVEC cells separated by a cell-impermeable membrane reduced the percentage of cardiomyocyte death following simulated ischaemia and reperfusion (sIR) from 80 ± 11% to 51 ± 4% (P < 0.05; N = 5). When EVs were removed from the HUVEC-conditioned medium it was no longer protective. Exosomes were purified from HUVEC-conditioned medium using differential centrifugation and characterized by nanoparticle tracking analysis, electron microscopy, and flow cytometry. Pre-incubation of cardiomyocytes with HUVEC exosomes reduced the percentage of cell death after sIR from 88 ± 4% to 55 ± 3% (P < 0.05; N = 3). This protection required ERK1/2 activity as it was prevented by inhibitors PD98059 and U0126. Ischaemic preconditioning caused about ~3-fold higher rate of exosome production from HUVEC and from isolated, perfused rat hearts. This increase resulted in significantly greater protection against sIR in cardiomyocytes. In conclusion, exosomes released from endothelial cells can confer resistance to sIR injury in cardiomyocytes via the activation of the ERK1/2 MAPK signalling pathway, and may contribute to IPC.

Indexed as

AnimalsApoptosisCoculture TechniquesExosomesFlavonoidsHumansHuman Umbilical Vein Endothelial CellsIschemic Preconditioning, MyocardialMaleMAP Kinase Signaling SystemMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Myocardial Reperfusion InjuryMyocytes, CardiacRatsRats, Sprague-Dawley2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneFlavonoidsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3

Identifiers

PMID30367147
PMCPMC6203728

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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.