Evidence map›Paper›PMID 30484954›Full record

ArticleJournal of cellular and molecular medicine2019

Exosomes from mesenchymal stem cells expressing miR-125b inhibit neointimal hyperplasia via myosin IE.

Dongqing Wang, Bin Gao, Jianing Yue, Fei Liu, Yifan Liu, Weiguo Fu, Yi Si

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 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
1.9field-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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
  2. Glycyrrhizic Acid Alleviates Atherosclerosis inInternational journal of molecular sciences · 2026
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  15. State of the field: cellular and exosomal therapeutic approaches in vascular regeneration.American journal of physiology. Heart and circulatory physiology · 2022
    Review
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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

7 authors at 1 institution in 1 country.

Dongqing WangDepartment of Vascular Surgery, Zhongshan Hospital Fudan University, Shanghai, China.
Bin GaoDepartment of Vascular Surgery, the Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China.
Jianing YueDepartment of Vascular Surgery, Zhongshan Hospital Fudan University, Shanghai, China.
Fei LiuDepartment of Vascular Surgery, Zhongshan Hospital Fudan University, Shanghai, China.
Yifan LiuDepartment of Vascular Surgery, Zhongshan Hospital Fudan University, Shanghai, China.
Weiguo FuDepartment of Vascular Surgery, Zhongshan Hospital Fudan University, Shanghai, China.
Yi SiDepartment of Vascular Surgery, Zhongshan Hospital Fudan University, Shanghai, China.ORCID 0000-0002-5637-0567
Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intercellular communication between mesenchymal stem cells (MSCs) and their target cells in the perivascular environment is modulated by exosomes derived from MSCs. However, the potential role of exosome-mediated microRNA transfer in neointimal hyperplasia remains to be investigated. To evaluate the effects of MSC-derived exosomes (MSC-Exo) on neointimal hyperplasia, their effects upon vascular smooth muscle cell (VSMC) growth in vitro and neointimal hyperplasia in vivo were assessed in a model of balloon-induced vascular injury. Our results showed that MSC-Exo were internalised by VSMCs and inhibited proliferation and migration in vitro. Further analysis revealed that miR-125b was enriched in MSC-Exo, and repressed the expression of myosin 1E (Myo1e) by targeting its 3' untranslated region. Additionally, MSC-Exo and exosomally transferred miR-125b repressed Myo1e expression and suppressed VSMC proliferation and migration and neointimal hyperplasia in vivo. In summary, our findings revealed that MSC-Exo can transfer miR-125b to VSMCs and inhibit VSMC proliferation and migration in vitro and neointimal hyperplasia in vivo by repressing Myo1e, indicating that miR-125b may be a therapeutic target in the treatment of vascular diseases.

Indexed as

AnimalsApoptosisCell MovementCell ProliferationExosomesGene Expression Regulation, DevelopmentalHumansHyperplasiaMesenchymal Stem CellsMesenchymal Stem Cell TransplantationMiceMicroRNAsMuscle, Smooth, VascularMyocytes, Smooth MuscleMyosin Type INeointimaMicroRNAsMirn125 microRNA, mouseMyo1e protein, mouseMyosin Type Iexosomemesenchymal stem cellsmiR-125bMyo1eneointimal hyperplasia

Identifiers

PMID30484954
PMCPMC6349157
OpenAlexW2902487039

What OpenQuestion holds

Textmetadata
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.