Evidence map›Paper›PMID 32371945›Full record

ArticleCell death & disease2020

Exosomal miR-25-3p from mesenchymal stem cells alleviates myocardial infarction by targeting pro-apoptotic proteins and EZH2.

Yi Peng, Ji-Ling Zhao, Zhi-Yong Peng, Wei-Fang Xu, Guo-Long Yu

Erratum issuedOpen access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 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 110 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed, 2 pooled it
8.5field-weighted citation impact, top 1% 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

110 citing papers in PubMed, 2 syntheses or guidelines pooled it, 164 citations in OpenAlex.

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Yi PengDepartment of Cardiology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan Province, P.R. China.
Ji-Ling ZhaoDepartment of Cardiology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan Province, P.R. China.
Zhi-Yong PengDepartment of Cardiology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan Province, P.R. China.
Wei-Fang XuDepartment of Cardiology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan Province, P.R. China.
Guo-Long YuDepartment of Cardiology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan Province, P.R. China. gl_y18@aliyun.com.ORCID http://orcid.org/0000-0002-0016-7770
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mesenchymal stem cell (MSC) therapy is a promising approach against myocardial infarction (MI). Studies have demonstrated that MSCs can communicate with other cells by secreting exosomes. In the present study, we aimed to identify exosomal microRNAs that might contribute to MSC-mediated cardioprotective effects. Primary cardiomyocytes were deprived of oxygen and glucose to mimic MI in vitro. For the animal model of MI, the left anterior descending artery was ligated for 1 h, followed by reperfusion for 12 h. MSC-derived exosomes were used to treat primary cardiomyocytes or mice. Cardioprotection-related microRNAs were determined, followed by target gene identification and functional studies with quantitative PCR, western blotting, MTT assay, flow cytometry assay, chromatin immunoprecipitation and dual-luciferase assay. We found that MSC co-culture reduced OGD-induced cardiomyocyte apoptosis and inflammatory responses. Cardioprotection was also observed upon treatment with MSC-derived exosomes in vitro and in vivo. In line with this, exosome uptake led to a significant increase in miR-25-3p in cardiomyocytes. Depletion of miR-25-3p in MSCs abolished the protective effects of exosomes. Mechanistically, miR-25-3p directly targeted the pro-apoptotic genes FASL and PTEN and reduced their protein levels. Moreover, miR-25-3p decreased the levels of EZH2 and H3K27me3, leading to derepression of the cardioprotective gene eNOS as well as the anti-inflammatory gene SOCS3. Inhibition of EZH2 or overexpression of miR-25-3p in cardiomyocytes was sufficient to confer cardioprotective effects in vitro and in vivo. We concluded that exosomal miR-25-3p from MSCs alleviated MI by targeting pro-apoptotic proteins and EZH2.

Indexed as

AnimalsApoptosisApoptosis Regulatory ProteinsCoculture TechniquesDisease Models, AnimalEnhancer of Zeste Homolog 2 ProteinExosomesMesenchymal Stem CellsMesenchymal Stem Cell TransplantationMice, Inbred BALB CMicroRNAsMyocardial InfarctionMyocytes, CardiacApoptosis Regulatory ProteinsEnhancer of Zeste Homolog 2 ProteinEzh2 protein, mouseMicroRNAsMIRN25 microRNA, mouse

Identifiers

PMID32371945
PMCPMC7200668
OpenAlexW3022897745

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.