Evidence map›Paper›PMID 27031991›Full record

ArticlePloS one2016

Endothelial Cells Can Regulate Smooth Muscle Cells in Contractile Phenotype through the miR-206/ARF6&NCX1/Exosome Axis.

Xiao Lin, Yu He, Xue Hou, Zhenming Zhang, Rui Wang, Qiong Wu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

34 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Mechanosensory entities and functionality of endothelial cells.Frontiers in cell and developmental biology · 2024
    Review
  6. Article
  7. Article
  8. Review
  9. Research progress on the mechanism of phenotypic transformation of pulmonary artery smooth muscle cells induced by hypoxia.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2022
    Review
  10. Review
  11. Article
  12. Article
  13. Extracellular vesicles in vascular remodeling.Acta pharmacologica Sinica · 2022
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. 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

6 authors at 2 institutions in 1 country.

Xiao LinMOE Key Laboratory of Bioinformatics, School of Life Sciences, Tsinghua University, Beijing 100084, China.
Yu HeMOE Key Laboratory of Bioinformatics, School of Life Sciences, Tsinghua University, Beijing 100084, China.
Xue HouDepartment of basic medicine, Medical College of Qinghai University, Xining 810016, China.
Zhenming ZhangMOE Key Laboratory of Bioinformatics, School of Life Sciences, Tsinghua University, Beijing 100084, China.
Rui WangMOE Key Laboratory of Bioinformatics, School of Life Sciences, Tsinghua University, Beijing 100084, China.
Qiong WuMOE Key Laboratory of Bioinformatics, School of Life Sciences, Tsinghua University, Beijing 100084, China.
Tsinghua University · CNQinghai University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Active interactions between endothelial cells and smooth muscle cells (SMCs) are critical to maintaining the SMC phenotype. Exosomes play an important role in intercellular communication. However, little is known about the mechanisms that regulate endothelial cells and SMCs crosstalk. We aimed to determine the mechanisms underlying the regulation of the SMC phenotype by human umbilical vein endothelial cells (HUVECs) through exosomes. We found that HUVECs overexpressing miR-206 upregulated contractile marker (α-SMA, Smoothelin and Calponin) mRNA expression in SMCs. We also found that the expression of miR-206 by HUVECs reduced exosome production by regulating ADP-Ribosylation Factor 6 (ARF6) and sodium/calcium exchanger 1 (NCX1). Using real-time PCR and western blot analysis, we showed that HUVEC-derived exosomes decreased the expression of contractile phenotype marker genes (α-SMA, Smoothelin and Calponin) in SMCs. Furthermore, a reduction of the miR-26a-containing exosomes secreted from HUVECs affects the SMC phenotype. We propose a novel mechanism in which miR-206 expression in HUVECs maintains the contractile phenotype of SMCs by suppressing exosome secretion from HUVECs, particularly miR-26a in exosomes, through targeting ARF6 and NCX1.

Indexed as

ADP-Ribosylation Factor 6ADP-Ribosylation FactorsCell CommunicationCoculture TechniquesEndothelial CellsExosomesGene ExpressionGene Expression RegulationHumansHuman Umbilical Vein Endothelial CellsMicroRNAsMyocytes, Smooth MuscleSignal TransductionSodium-Calcium ExchangerADP-Ribosylation Factor 6ADP-Ribosylation FactorsARF6 protein, humanMicroRNAsMIRN206 microRNA, humanSodium-Calcium Exchangersodium-calcium exchanger 1

Identifiers

PMID27031991
PMCPMC4816502
OpenAlexW2313103425

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.