Evidence map›Paper›PMID 32513275›Full record

ArticleStem cell research & therapy2020

Exosomes derived from mesenchymal stem cells inhibit neointimal hyperplasia by activating the Erk1/2 signalling pathway in rats.

Zhihui Liu, Chao Wu, Xinliang Zou, Weiming Shen, Jiacai Yang, Xiaorong Zhang, Xiaohong Hu, Haidong Wang, Yi Liao, Tao Jing

Open access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  14. Exosomes and cancer: from molecular mechanisms to clinical applications.Medical oncology (Northwood, London, England) · 2021
    Review
  15. BioMed research international · 2021
    Article
  16. Review
  17. 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

10 authors at 3 institutions in 1 country.

Zhihui LiuDepartment of Cardiology, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, 400038, China.
Chao WuState Key Laboratory of Silkworm Genome Biology, The Institute of Sericulture and Systems Biology, Southwest University, Chongqing, China.
Xinliang ZouDepartment of Cardiology, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, 400038, China.
Weiming ShenLaboratory of Integrative Medicine, School of Basic Medical Sciences, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Jiacai YangThe Institute of Burn Research, South-West Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
Xiaorong ZhangThe Institute of Burn Research, South-West Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
Xiaohong HuThe Institute of Burn Research, South-West Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
Haidong WangDepartment of Thoracic Surgery, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
Yi LiaoDepartment of Thoracic Surgery, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
Tao JingDepartment of Cardiology, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, 400038, China. xnkjt@sohu.com.
Army Medical University · CNSouthwest Hospital · CNShanghai University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRestenosis is a serious problem in patients who have undergone percutaneous transluminal angioplasty. Endothelial injury resulting from surgery can lead to endothelial dysfunction and neointimal formation by inducing aberrant proliferation and migration of vascular smooth muscle cells. Exosomes secreted by mesenchymal stem cells have been a hot topic in cardioprotective research. However, to date, exosomes derived from mesenchymal stem cells (MSC-Exo) have rarely been reported in association with restenosis after artery injury. The aim of this study was to investigate whether MSC-Exo inhibit neointimal hyperplasia in a rat model of carotid artery balloon-induced injury and, if so, to explore the underlying mechanisms.

methodsCharacterization of MSC-Exo immunophenotypes was performed by electron microscopy, nanoparticle tracking analysis and western blot assays. To investigate whether MSC-Exo inhibited neointimal hyperplasia, rats were intravenously injected with normal saline or MSC-Exo after carotid artery balloon-induced injury. Haematoxylin-eosin staining was performed to examine the intimal and media areas. Evans blue dye staining was performed to examine re-endothelialization. Moreover, immunohistochemistry and immunofluorescence were performed to examine the expression of CD31, vWF and α-SMA. To further investigate the involvement of MSC-Exo-induced re-endothelialization, the underlying mechanisms were studied by cell counting kit-8, cell scratch, immunofluorescence and western blot assays.

resultsOur data showed that MSC-Exo were ingested by endothelial cells and that systemic injection of MSC-Exo suppressed neointimal hyperplasia after artery injury. The Evans blue staining results showed that MSC-Exo could accelerate re-endothelialization compared to the saline group. The immunofluorescence and immunohistochemistry results showed that MSC-Exo upregulated the expression of CD31 and vWF but downregulated the expression of α-SMA. Furthermore, MSC-Exo mechanistically facilitated proliferation and migration by activating the Erk1/2 signalling pathway. The western blot results showed that MSC-Exo upregulated the expression of PCNA, Cyclin D1, Vimentin, MMP2 and MMP9 compared to that in the control group. Interestingly, an Erk1/2 inhibitor reversed the expression of the above proteins.

conclusionOur data suggest that MSC-Exo can inhibit neointimal hyperplasia after carotid artery injury by accelerating re-endothelialization, which is accompanied by activation of the Erk1/2 signalling pathway. Importantly, our study provides a novel cell-free approach for the treatment of restenosis diseases after intervention.

Indexed as

Carotid Artery InjuriesExosomesMesenchymal Stem CellsAnimalsCell ProliferationEndothelial CellsHumansHyperplasiaRatsEndothelial cellsErk1/2 signalling pathwayMSC-ExoNeointimal hyperplasiaRe-endothelializationRestenosis

Identifiers

PMID32513275
PMCPMC7278178
OpenAlexW3033224963

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.