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MiR-7015-3p Targets Nuclear Factor-Kappa-B-Inhibitor Alpha to Aggravate Hypoxia/Reoxygenation Injury in

Xin Shen1, Jing Tao1, Zhao Wang1

  • 1Department of Cardiology, People's Hospital of Xinjiang Uygur Autonomous Region.

International Heart Journal
|October 2, 2022
PubMed

Insights

MicroRNA-7015 (miR-7015) worsens heart injury from ischemia-reperfusion (I/R) by suppressing Nfkbia. Inhibiting miR-7015 protects heart cells by restoring Nfkbia levels, offering a potential therapeutic target for I/R injury.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Cellular Physiology

Background:

  • Ischemic heart disease (IHD) is a leading cause of mortality worldwide.
  • Myocardial ischemia-reperfusion (I/R) injury is a critical complication following heart attacks and cardiac surgery.
  • Understanding the molecular mechanisms of I/R injury is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the role of microRNA-7015 (miR-7015) in hypoxia-reoxygenation (H/R)-induced cardiomyocyte injury.
  • To identify the downstream targets and signaling pathways regulated by miR-7015 in the context of cardiac injury.
  • To explore the potential of targeting the miR-7015/Nfkbia axis for therapeutic intervention in I/R injury.

Main Methods:

  • Establishment of a hypoxia-reoxygenation (H/R) model using isolated cardiomyocytes.
  • Overexpression and inhibition of miR-7015 in cardiomyocytes to assess its effects on H/R injury.
  • Analysis of cell viability, apoptosis, and cytokine release.
  • Bioinformatic analysis and experimental validation to identify miR-7015 targets, focusing on nuclear factor-kappa-B-inhibitor alpha (Nfkbia).
  • Overexpression of Nfkbia to evaluate its protective effects against H/R injury and its interaction with miR-7015.

Main Results:

  • miR-7015 was found to be upregulated in myocardial tissues and cardiomyocytes following I/R and H/R injury, respectively.
  • Overexpression of miR-7015 exacerbated H/R-induced cardiomyocyte injury, while its inhibition ameliorated the injury.
  • miR-7015 directly targets and inhibits the expression of Nfkbia.
  • Overexpression of Nfkbia protected cardiomyocytes against H/R injury and partially reversed the detrimental effects of miR-7015 overexpression.

Conclusions:

  • The miR-7015/Nfkbia axis plays a significant role in modulating cardiomyocyte injury induced by H/R.
  • miR-7015 exacerbates cardiac injury by downregulating Nfkbia, likely through the NF-κB signaling pathway.
  • Targeting the miR-7015/Nfkbia interaction presents a potential therapeutic strategy for mitigating myocardial I/R injury.

Keywords:
Ischemic heart disease (IHD)MicroRNAs (miRNAs)Myocardial ischemia/reperfusion (I/R) injuryNF-κB signaling

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