Evidence map›Paper›PMID 25838349›Full record

ArticleBlood2015

Endothelial cells suppress monocyte activation through secretion of extracellular vesicles containing antiinflammatory microRNAs.

Makon-Sébastien Njock, Henry S Cheng, Lan T Dang, Maliheh Nazari-Jahantigh, Andrew C Lau, Emilie Boudreau, Mark Roufaiel, Myron I Cybulsky, Andreas Schober, Jason E Fish

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

Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 182 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
182citing papers in PubMed, 5 pooled it
8.7field-weighted citation impact, top 2% 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

182 citing papers in PubMed, 5 syntheses or guidelines pooled it, 266 citations in OpenAlex.

  1. Pooled it
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  5. Guideline
  6. Investigating Dietary microRNA Stability and Function Using a Transgenic Milk Model With Unique microRNA Sequences.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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122 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

10 authors at 5 institutions in 2 countries.

Makon-Sébastien NjockToronto General Research Institute, University Health Network, Toronto, ON, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada; Heart and Stroke Richard Lewar Centre of Excellence in Cardiovascular Research, Toronto, ON, Canada;
Henry S ChengToronto General Research Institute, University Health Network, Toronto, ON, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada; Heart and Stroke Richard Lewar Centre of Excellence in Cardiovascular Research, Toronto, ON, Canada;
Lan T DangToronto General Research Institute, University Health Network, Toronto, ON, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada; Heart and Stroke Richard Lewar Centre of Excellence in Cardiovascular Research, Toronto, ON, Canada;
Maliheh Nazari-JahantighInstitute for Cardiovascular Prevention, Ludwig-Maximilians-University Munich, Munich, Germany; and.
Andrew C LauToronto General Research Institute, University Health Network, Toronto, ON, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada; Heart and Stroke Richard Lewar Centre of Excellence in Cardiovascular Research, Toronto, ON, Canada;
Emilie BoudreauToronto General Research Institute, University Health Network, Toronto, ON, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada; Heart and Stroke Richard Lewar Centre of Excellence in Cardiovascular Research, Toronto, ON, Canada;
Mark RoufaielToronto General Research Institute, University Health Network, Toronto, ON, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada; Heart and Stroke Richard Lewar Centre of Excellence in Cardiovascular Research, Toronto, ON, Canada;
Myron I CybulskyToronto General Research Institute, University Health Network, Toronto, ON, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada; Heart and Stroke Richard Lewar Centre of Excellence in Cardiovascular Research, Toronto, ON, Canada;
Andreas SchoberInstitute for Cardiovascular Prevention, Ludwig-Maximilians-University Munich, Munich, Germany; and DZHK (German Center for Cardiovascular Research), Partner Site Munich Heart Alliance, Munich, Germany.
Jason E FishToronto General Research Institute, University Health Network, Toronto, ON, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada; Heart and Stroke Richard Lewar Centre of Excellence in Cardiovascular Research, Toronto, ON, Canada;
University Health Network · CAHeart and Stroke Foundation · CAGerman Centre for Cardiovascular Research · DELudwig-Maximilians-Universität München · DEUniversity of Toronto · CA

Funding

Canadian Institutes of Health Research MTA-118968
6 · The paper itself

Abstract

The blood contains high concentrations of circulating extracellular vesicles (EVs), and their levels and contents are altered in several disease states, including cardiovascular disease. However, the function of circulating EVs, especially the microRNAs (miRNAs) that they contain, are poorly understood. We sought to determine the effect of secreted vesicles produced by quiescent endothelial cells (ECs) on monocyte inflammatory responses and to assess whether transfer of microRNAs occurs between these cells. We observed that monocytic cells cocultured (but not in contact) with ECs were refractory to inflammatory activation. Further characterization revealed that endothelium-derived EVs (EC-EVs) suppressed monocyte activation by enhancing immunomodulatory responses and diminishing proinflammatory responses. EVs isolated from mouse plasma also suppressed monocyte activation. Importantly, injection of EC-EVs in vivo repressed monocyte/macrophage activation, confirming our in vitro findings. We found that several antiinflammatory microRNAs were elevated in EC-EV-treated monocytes. In particular, miR-10a was transferred to monocytic cells from EC-EVs and could repress inflammatory signaling through the targeting of several components of the NF-κB pathway, including IRAK4. Our findings reveal that ECs secrete EVs that can modulate monocyte activation and suggest that altered EV secretion and/or microRNA content may affect vascular inflammation in the setting of cardiovascular disease.

Indexed as

Cell CommunicationCell LineCoculture TechniquesEndothelial CellsExtracellular SpaceHumansInflammationInterferon Regulatory FactorsLipopolysaccharidesMicroRNAsMonocytesNF-kappa BSecretory VesiclesSignal TransductionInterferon Regulatory FactorsIRF5 protein, humanLipopolysaccharidesMicroRNAsNF-kappa B

Identifiers

PMID25838349
PMCPMC4440888
OpenAlexW2076102211

What OpenQuestion holds

Textmetadata
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.