Evidence map›Paper›PMID 32944170›Full record

ArticleJournal of extracellular vesicles2020

Endothelial cell-derived extracellular vesicles alter vascular smooth muscle cell phenotype through high-mobility group box proteins.

Michael J Boyer, Yayoi Kimura, Tomoko Akiyama, Ariele Y Baggett, Kyle J Preston, Rosario Scalia, Satoru Eguchi, Victor Rizzo

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Journal of extracellular vesicles, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

65 citing papers in PubMed, 75 citations in OpenAlex.

  1. Cellular crosstalk between endothelial and vascular smooth muscle cells via the BACH1/COL3A1 axis promotes vascular calcification in chronic kidney disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  2. Review
  3. Review
  4. The role of HMGB1 in vascular endothelial cells.Apoptosis : an international journal on programmed cell death · 2026
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Michael J BoyerCardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.
Yayoi KimuraAdvanced Medical Research Center, Yokohama City University, Yokohama, Japan.
Tomoko AkiyamaAdvanced Medical Research Center, Yokohama City University, Yokohama, Japan.
Ariele Y BaggettCardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.
Kyle J PrestonCardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.
Rosario ScaliaCardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.
Satoru EguchiCardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.
Victor RizzoCardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.ORCID https://orcid.org/0000-0002-5705-5462
Temple University · USYokohama City University Medical Center · JP

Funding

Inflammatory Responses of The Visceral Adipose Tissue MicrocirculationR01DK111042 · NIDDK · TEMPLE UNIV OF THE COMMONWEALTH · PI EGUCHI, SATORU, SCALIA, ROSARIO G · 2017 to 2020
$2.3M
EGF-ADAM17 axis in the pathophysiology of intracranial aneurysmR01NS109382 · NINDS · ST. JOSEPH'S HOSPITAL AND MEDICAL CENTER · PI EGUCHI, SATORU, HASHIMOTO, TOMOKI · 2019 to 2023
$2.2M
Mechanism of Hypertensive Vascular Remodeling and End-Organ DamageR01HL133248 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI EGUCHI, SATORU · 2016 to 2019
$1.8M
Vascular signal as a therapeutic target for abdominal aortic aneurysmR01HL128324 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI EGUCHI, SATORU, RIZZO, VICTOR J. · 2015 to 2018
$1.6M
NHLBI NIH HHS R01 HL128324NHLBI NIH HHS R01 HL133248NIDDK NIH HHS R01 DK111042NINDS NIH HHS R01 NS109382
6 · The paper itself

Abstract

The vascular endothelium and smooth muscle form adjacent cellular layers that comprise part of the vascular wall. Each cell type can regulate the other's structure and function through a variety of paracrine effectors. Extracellular vesicles (EVs) are released from and transit between cells constituting a novel means of cell-cell communication. Here, we characterized the proteome of EVs released from each vascular cell type and examined the extent to which these vesicles participate in endothelial-vascular smooth muscle cell (VSMC) communication. EVs were collected by ultracentrifugation from media of rat aortic endothelial and smooth muscle cells cultured under serum-free conditions. Vesicle morphology, size and concentration were evaluated by transmission electron microscopy and nanoparticle tracking analysis. Western blot as well as shot gun proteomic analyses revealed sets of proteins common to both endothelial- and smooth muscle-derived EVs as well as proteins unique to each vascular cell type. Functionally, endothelial-derived EVs stimulated vascular cell adhesion molecule-1 (VCAM-1) expression and enhanced leukocyte adhesion in VSMCs while smooth muscle EVs did not elicit similar effects in endothelial cells (ECs). EVs from ECs also induced protein synthesis and senescence in VSMCs. Proteomic analysis of VSMCs following exposure to EC-derived EVs revealed upregulation of several proteins including pro-inflammatory molecules, high-mobility group box (HMGB) 1 and HMGB2. Pharmacological blockade HMGB1 and HMGB2 and siRNA depletion of HMGB1 in smooth muscle cells attenuated VCAM-1 expression and leukocyte adhesion induced by EC EVs. These data suggest that EC-derived EVs can enhance signalling pathways which influence smooth muscle cell phenotype.

Indexed as

endothelial cellsexosomeExtracellular vesicleshigh-mobility group box 1proteomicsvascular smooth muscle cells

Identifiers

PMID32944170
PMCPMC7480479
OpenAlexW3036255021

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.