Open Access

MicroRNA‑138 attenuates myocardial ischemia reperfusion injury through inhibiting mitochondria‑mediated apoptosis by targeting HIF1‑α

  • Authors:
    • Yan Liu
    • Jianfeng Zou
    • Xiaoyan Liu
    • Quan Zhang
  • View Affiliations

  • Published online on: September 5, 2019     https://doi.org/10.3892/etm.2019.7976
  • Pages: 3325-3332
  • Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Myocardial ischemia‑reperfusion (I/R) injury is considered to have a detrimental role in coronary heart disease, which is considered to be the leading cause of death worldwide. However, the molecular mechanism involved in the progression of myocardial I/R injury is still unclear. The current study aimed to investigate the expression and function of microRNA (miR)‑138 in the process of myocardial I/R injury. First, miR‑138 expression levels were analyzed both in myocardium with I/R injury and control myocardium using reverse transcription‑quantitative polymerase chain reaction analysis. Then, the relationship between the levels of miR‑138 and hypoxia‑inducible factor (HIF)1‑α was also investigated using a luciferase reporter assay. Assessment of myocardial infarct size, measurements of serum myocardial enzymes and electron microscopy analysis were all utilized to analyse the effect of miR‑138 on myocardial I/R injury. The authors of current study also used western blotting to examine the expression levels of the mitochondrial fission‑related proteins dynamin‑1‑like protein and mitochondrial fission 1 protein. It was found that miR‑138 is downregulated and HIF1‑α is upregulated after myocardial ischemia reperfusion injury. Overexpression of miR‑138 reduced myocardial I/R injury‑induced infarct sizes and myocardial enzyme levels, and it also inhibited the expression of proteins related to mitochondrial morphology and myocardial I/R‑induced mitochondrial apoptosis by targeting HIF1‑α. Taken together, these findings provide a novel insight into the molecular mechanism of miR‑138 and HIF1‑α in the progression of myocardial I/R injury. miR‑138 has the potential to become a promising therapeutic target for treating myocardial I/R injury.
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November-2019
Volume 18 Issue 5

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Liu Y, Zou J, Liu X and Zhang Q: MicroRNA‑138 attenuates myocardial ischemia reperfusion injury through inhibiting mitochondria‑mediated apoptosis by targeting HIF1‑α. Exp Ther Med 18: 3325-3332, 2019.
APA
Liu, Y., Zou, J., Liu, X., & Zhang, Q. (2019). MicroRNA‑138 attenuates myocardial ischemia reperfusion injury through inhibiting mitochondria‑mediated apoptosis by targeting HIF1‑α. Experimental and Therapeutic Medicine, 18, 3325-3332. https://doi.org/10.3892/etm.2019.7976
MLA
Liu, Y., Zou, J., Liu, X., Zhang, Q."MicroRNA‑138 attenuates myocardial ischemia reperfusion injury through inhibiting mitochondria‑mediated apoptosis by targeting HIF1‑α". Experimental and Therapeutic Medicine 18.5 (2019): 3325-3332.
Chicago
Liu, Y., Zou, J., Liu, X., Zhang, Q."MicroRNA‑138 attenuates myocardial ischemia reperfusion injury through inhibiting mitochondria‑mediated apoptosis by targeting HIF1‑α". Experimental and Therapeutic Medicine 18, no. 5 (2019): 3325-3332. https://doi.org/10.3892/etm.2019.7976