Evidence map›Paper›PMID 30516028›Full record

ArticleJournal of cellular and molecular medicine2019

Ischaemia alters the effects of cardiomyocyte-derived extracellular vesicles on macrophage activation.

Rafael Almeida Paiva, Tania Martins-Marques, Katia Jesus, Teresa Ribeiro-Rodrigues, Monica Zuzarte, Ana Silva, Liliana Reis, Maria da Silva, Paulo Pereira, Pieter Vader and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 16% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Pooled it
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  14. Article
  15. Communications between macrophages and cardiomyocytes.Cell communication and signaling : CCS · 2023
    Review
  16. Review
  17. Review
  18. Extracellular Vesicles and Ischemic Cardiovascular Diseases.Advances in experimental medicine and biology · 2023
    Article
  19. Review
  20. Intercellular transfer of miR-200c-3p impairs the angiogenic capacity of cardiac endothelial cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
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

14 authors at 3 institutions in 2 countries.

Rafael Almeida PaivaCoimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, University of Coimbra, Coimbra, Portugal.
Tania Martins-MarquesCoimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, University of Coimbra, Coimbra, Portugal.
Katia JesusCoimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, University of Coimbra, Coimbra, Portugal.
Teresa Ribeiro-RodriguesCoimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, University of Coimbra, Coimbra, Portugal.
Monica ZuzarteCoimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, University of Coimbra, Coimbra, Portugal.
Ana SilvaCNC.IBILI, University of Coimbra, Coimbra, Portugal.
Liliana ReisCardiology Department, CHUC-HG, Coimbra, Portugal.
Maria da SilvaCardiology Department, CHUC-HG, Coimbra, Portugal.
Paulo PereiraChronic Diseases Research Center (CEDOC), NOVA Medical School, Faculdade de Ciências Médicas, Universidade NOVA de Lisboa, Lisboa, Portugal.
Pieter VaderDepartment of Experimental Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands.
Joost Petrus Gerardus SluijterDepartment of Cardiology, Division of Heart & Lungs, University Medical Center Utrecht, Utrecht, The Netherlands.
Lino GonçalvesCoimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, University of Coimbra, Coimbra, Portugal.
Maria Teresa CruzCNC.IBILI, University of Coimbra, Coimbra, Portugal.
Henrique GiraoCoimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, University of Coimbra, Coimbra, Portugal.ORCID 0000-0002-5786-8447
University of Coimbra · PTUniversity Medical Center Utrecht · NLUniversidade Nova de Lisboa · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial ischaemia is associated with an exacerbated inflammatory response, as well as with a deregulation of intercellular communication systems. Macrophages have been implicated in the maintenance of heart homeostasis and in the progression and resolution of the ischaemic injury. Nevertheless, the mechanisms underlying the crosstalk between cardiomyocytes and macrophages remain largely underexplored. Extracellular vesicles (EVs) have emerged as key players of cell-cell communication in cardiac health and disease. Hence, the main objective of this study was to characterize the impact of cardiomyocyte-derived EVs upon macrophage activation. Results obtained demonstrate that EVs released by H9c2 cells induced a pro-inflammatory profile in macrophages, via p38MAPK activation and increased expression of iNOS, IL-1β and IL-6, being these effects less pronounced with ischaemic EVs. EVs derived from neonatal cardiomyocytes, maintained either in control or ischaemia, induced a similar pattern of p38MAPK activation, expression of iNOS, IL-1β, IL-6, IL-10 and TNFα. Importantly, adhesion of macrophages to fibronectin was enhanced by EVs released by cardiomyocytes under ischaemia, whereas phagocytic capacity and adhesion to cardiomyocytes were higher in macrophages incubated with control EVs. Additionally, serum-circulating EVs isolated from human controls or acute myocardial infarction patients induce macrophage activation. According to our model, in basal conditions, cardiomyocyte-derived EVs maintain a macrophage profile that ensure heart homeostasis, whereas during ischaemia, this crosstalk is affected, likely impacting healing and post-infarction remodelling.

Indexed as

AgedAnimalsCell LineExtracellular VesiclesFemaleHumansInflammationInterleukin-10Interleukin-1betaInterleukin-6IschemiaMacrophage ActivationMacrophagesMaleMiddle AgedMyocardial InfarctionInterleukin-10Interleukin-1betaInterleukin-6Nitric Oxide Synthase Type IIp38 Mitogen-Activated Protein KinasesTumor Necrosis Factor-alphaacute myocardial infarctioncardiomyocytesextracellular vesiclesintercellular communicationmacrophages

Identifiers

PMID30516028
PMCPMC6349194
OpenAlexW2903567039

What OpenQuestion holds

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LicenceCC BY
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.