Evidence map›Paper›PMID 28662151›Full record

ArticlePloS one2017

Bone marrow mesenchymal stem cell-derived vascular endothelial growth factor attenuates cardiac apoptosis via regulation of cardiac miRNA-23a and miRNA-92a in a rat model of myocardial infarction.

Yi-Sun Song, Hyun-Woo Joo, In-Hwa Park, Guang-Yin Shen, Yonggu Lee, Jeong Hun Shin, Hyuck Kim, Kyung-Soo Kim

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

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 15% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
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  6. The Role of ncRNAs in Cardiac Infarction and Regeneration.Journal of cardiovascular development and disease · 2023
    Review
  7. Article
  8. Study of the Association betweenJournal of personalized medicine · 2022
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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

8 authors at 2 institutions in 1 country.

Yi-Sun SongGraduate School of Biomedical Science and Engineering, Hanyang University, Seoul, South Korea.
Hyun-Woo JooGraduate School of Biomedical Science and Engineering, Hanyang University, Seoul, South Korea.
In-Hwa ParkGraduate School of Biomedical Science and Engineering, Hanyang University, Seoul, South Korea.
Guang-Yin ShenDepartment of Internal Medicine, Hanyang University College of Medicine, Seoul, South Korea.
Yonggu LeeDepartment of Internal Medicine, Hanyang University Guri Hospital, Guri, South Korea.
Jeong Hun ShinDepartment of Internal Medicine, Hanyang University Guri Hospital, Guri, South Korea.
Hyuck KimDepartment of Thoracic and Cardiovascular Surgery, Hanyang University College of Medicine, Seoul, South Korea.
Kyung-Soo KimGraduate School of Biomedical Science and Engineering, Hanyang University, Seoul, South Korea.ORCID http://orcid.org/0000-0002-0891-1023
Hanyang University · KRHanyang University Guri Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone marrow-mesenchymal stem cell (BM-MSC) therapy improves the recovery of cardiac function after myocardial infarction (MI); however, the underlying molecular mechanisms are not completely understood. Recent studies have shown that microRNAs (miRNAs) modulate the pathophysiology of cardiovascular diseases. Here, we investigated the mechanisms underlying the effects of BM-MSC-derived paracrine factors and cardiac miRNAs on myocardial regeneration after MI. In our study, MI was induced by permanent ligation of the left anterior descending (LAD) coronary artery. BM-MSCs transplanted in infarcted rats significantly downregulated the expression of miRNA-23a and miRNA-92a and inhibited apoptosis in the myocardium. An in vitro experiment showed that supernatant from BM-MSCs cultured under hypoxia contained higher levels of vascular endothelial growth factor (VEGF) than that from BM-MSCs under normoxia. In addition, inhibition of miRNA-23a and miRNA-92a reduced cardiac apoptosis. Moreover, the VEGF-containing BM-MSC supernatant inhibited miRNA-23a and miRNA-92a expression and reduced apoptotic signaling in cardiomyocytes under hypoxia. These effects were inhibited when the supernatant was treated with neutralizing antibodies against VEGF. Our results indicate that the paracrine factor, VEGF, derived from transplanted BM-MSCs, regulated the expression of miRNAs such as miRNA-23a and miRNA-92a and exerted anti-apoptotic effects in cardiomyocytes after MI.

Indexed as

Disease Models, AnimalAnimalsApoptosisBone Marrow CellsCells, CulturedCulture Media, ConditionedMesenchymal Stem CellsMicroRNAsMyocardial InfarctionMyocardiumMyocytes, CardiacRatsVascular Endothelial Growth Factor ACulture Media, ConditionedMicroRNAsMIRN23a microRNA, ratMIRN92 microRNA, ratVascular Endothelial Growth Factor A

Identifiers

PMID28662151
PMCPMC5491110
OpenAlexW2729533505

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.