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Cited by 53Mesenchymal stem cell researchCardiac Fibrosis and RemodelingCongenital heart defects research

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

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Song, Yi-Sun, Joo, Hyun-Woo, Park, In-Hwa, Shen, Guang-Yin, Lee, Yonggu, Shin, Jeong Hun, Kim, Hyuck, Kim, Kyung-Soo·2017·PLOS ONE
DOI 10.1371/journal.pone.0179972PMC PMC5491110
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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.

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  • In a rat model of myocardial infarction, miR-23a expression in the heart is concerned with modulation of VEGF derived from bone marrow mesenchymal stem cell therapy, improving cardiac function impairment caused by myocardial infarction through reducing cellular apoptosis.

    “In another rat model of myocardial infarction, it was observed that the expression level of miR-23a in the heart is concerned with the modulation of VEGF derived from bone marrow mesenchymal stem cell (BM-MSC) therapy, improving cardiac function impairment caused by myocardial infarction through reducing cellular apoptosis [58].”

    From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [58]

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References 60 · Cited by 53

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Authors
Song, Y.-S., Joo, H.-W., Park, I.-H., Shen, G.-Y., Lee, Y., Shin, J. H., Kim, H., & Kim, K.-S.
Affiliations
  • Hanyang University (KR)
  • Hanyang University Guri Hospital (KR)
Corresponding author
Kim, Kyung-Soo
ORCID
Venue
PLOS ONE
Publisher
Public Library of Science (PLoS)
Published
2017-06-29
Volume
12
Issue
6
Pages
e0179972
ISSN
1932-6203 (ISSN-L)
DOI
10.1371/journal.pone.0179972
PMC
PMC5491110
OpenAlex
W2729533505
Cited by
53
References
60
Citations by year
2026: 3 · 2025: 2 · 2024: 3 · 2023: 4 · 2022: 8 · 2021: 9 · 2020: 12 · 2019: 9 · 2018: 3
FWCI
3.77
Type
journal article
Language
en
Open access
Licence
Locations
  • PLoS ONE (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Figshare (submittedVersion, cc-by)
Funders
  • National Research Foundation
  • National Research Foundation of Korea (2015R1D1A1A02062008)
Topics
  • Health Sciences › Medicine › Genetics › Mesenchymal stem cell research
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
Keywords
bone marrow mesenchymal stem cells, vascular endothelial growth factor, myocardial infarction, cardiac apoptosis, paracrine signaling, cardiomyocyte hypoxia, microRNA regulation, stem cell therapy, cardiac regeneration
MeSH terms
Animals, Bone Marrow Cells, Cells, Cultured, Disease Models, Animal, Myocardial Infarction, Myocardium, Culture Media, Conditioned, Apoptosis, Myocytes, Cardiac, MicroRNAs, Vascular Endothelial Growth Factor A, Rats, Mesenchymal Stem Cells

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