Open Access

miR‑155 inhibition represents a potential valuable regulator in mitigating myocardial hypoxia/reoxygenation injury through targeting BAG5 and MAPK/JNK signaling

  • Authors:
    • Jing Xi
    • Qiang‑Qiang Li
    • Bing‑Qiang Li
    • Ning Li
  • View Affiliations

  • Published online on: January 9, 2020     https://doi.org/10.3892/mmr.2020.10924
  • Pages: 1011-1020
  • Copyright: © Xi et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Increasing evidence has indicated that miR‑155 is closely associated with apoptosis, which may protect the myocardium and diminish the infarct area in myocardial ischemia reperfusion injury (IRI). In addition, studies have revealed that miR‑155 serves a leading role in promoting fibroblast inflammation, cardiac dysfunction and other aspects of myocardial injury. The present study aimed to uncover the function and potential biological mechanism of miR‑155 in myocardial IRI. The rat H9c2 myocardial cells was treated with hypoxia/reoxygenation (H/R) to simulate IRI in vitro. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) was used to detect the expression levels of miR‑155 mRNA. Cell Counting Kit‑8 and flow cytometry assays and western blot analysis were applied to determine the biological behaviors of the H/R‑treated cells. The association between miR‑155 and BAG family molecular chaperone regulator 5 (BAG5) was predicted by bioinformatics software and was confirmed by dual luciferase assay. RT‑qPCR and western blot analysis were used to analyze the expression of BAG5. The key proteins involved in mitogen‑activated protein kinase (MAPK)/JNK signaling pathway were detected by western blot analysis. The data from the RT‑qPCR assay indicated that the expression of miR‑155 was markedly upregulated in the H/R model, and that downregulation of miR‑155 may promote cell proliferation and inhibit cell apoptosis, and vice versa. BAG5, which was downregulated in the H/R model, was confirmed as a target of miR‑155 and negatively modulated by miR‑155. The key proteins involved in MAPK/JNK signaling, which were highly expressed in the H/R model, were suppressed by treatment with the miR‑155 inhibitor, and overexpression of BAG5 promoted the protective effect of miR‑155 inhibition on cell injury caused by H/R. In addition, the expression patterns of hypoxia‑inducible factor 1‑α and von Hippel‑Lindau were altered following different treatments. Taken together, the data from the present study indicated that miR‑155 inhibition represented a potential treatment strategy to improve myocardial H/R injury, which may be associated with targeting BAG5 and inhibition of the MAPK/JNK pathway.
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March 2020
Volume 21 Issue 3

Print ISSN: 1791-2997
Online ISSN:1791-3004

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APA
Xi, J., Li, Q., Li, B., & Li, N. (2020). miR‑155 inhibition represents a potential valuable regulator in mitigating myocardial hypoxia/reoxygenation injury through targeting BAG5 and MAPK/JNK signaling. Molecular Medicine Reports, 21, 1011-1020. https://doi.org/10.3892/mmr.2020.10924
MLA
Xi, J., Li, Q., Li, B., Li, N."miR‑155 inhibition represents a potential valuable regulator in mitigating myocardial hypoxia/reoxygenation injury through targeting BAG5 and MAPK/JNK signaling". Molecular Medicine Reports 21.3 (2020): 1011-1020.
Chicago
Xi, J., Li, Q., Li, B., Li, N."miR‑155 inhibition represents a potential valuable regulator in mitigating myocardial hypoxia/reoxygenation injury through targeting BAG5 and MAPK/JNK signaling". Molecular Medicine Reports 21, no. 3 (2020): 1011-1020. https://doi.org/10.3892/mmr.2020.10924