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Long noncoding RNA AK088388 regulates autophagy through miR-30a to affect cardiomyocyte injury

Jing-Jing Wang1,2, Zi-Dong Bie3, Chao-Feng Sun4

  • 1Department of Medicine, Xi'an Jiaotong University, Xi'an, Shanxi, China.

Journal of Cellular Biochemistry
|January 13, 2019
PubMed

Insights

Long noncoding RNA (lncRNA) AK088388 exacerbates myocardial ischemia/reperfusion injury by competitively binding to miR-30a, promoting autophagy and cell damage. Inhibiting AK088388 or enhancing miR-30a protects cardiomyocytes.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • RNA Biology

Background:

  • Myocardial ischemia/reperfusion (I/R) injury is a significant complication of myocardial infarction.
  • Long noncoding RNAs (lncRNAs) and autophagy are implicated in cardiovascular disease pathogenesis.
  • Understanding the molecular mechanisms underlying I/R injury is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the role of the lncRNA AK088388 and microRNA miR-30a in myocardial I/R injury.
  • To elucidate the molecular interaction between AK088388, miR-30a, and autophagy-related proteins.
  • To evaluate the therapeutic potential of targeting the AK088388/miR-30a axis in protecting cardiomyocytes from I/R injury.

Main Methods:

  • Bioinformatic analysis and dual-luciferase reporter assays to predict and validate binding sites.
  • Quantitative real-time PCR to assess gene and microRNA expression levels.
  • In vitro experiments using hypoxia/reoxygenation (H/R) treated cardiomyocytes, including cell viability assays, lactate dehydrogenase release assays, and apoptosis assays.
  • RNA interference and mimic transfection to modulate gene and microRNA expression.

Main Results:

  • miR-30a directly binds to both AK088388 and Beclin-1.
  • miR-30a expression is downregulated, while AK088388, Beclin-1, and LC3-II expression is upregulated in H/R cardiomyocytes.
  • AK088388 promotes Beclin-1 and LC3-II expression and autophagy, exacerbating H/R-induced cardiomyocyte damage.
  • Inhibition of AK088388 or augmentation of miR-30a enhances cardiomyocyte viability and reduces apoptosis and LDH release.

Conclusions:

  • AK088388 acts as a competing endogenous RNA (ceRNA) that sponges miR-30a, leading to increased autophagy and cell death in myocardial I/R injury.
  • The AK088388/miR-30a axis represents a novel therapeutic target for mitigating myocardial I/R injury.
  • Targeting this pathway offers a promising strategy for protecting the heart during ischemic events.
Keywords:
autophagycardiomyocytelong noncoding RNA (lncRNA)miR-30amyocardial infarction

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