MicroRNA-98 attenuates cardiac ischemia-reperfusion injury through inhibiting DAPK1 expression

Chang-Lin Zhai1,2, Guan-Min Tang2, Gang Qian2

  • 1Department of Cardiovascular Diseases, Xinhua Hospital, Shanghai Jiaotong University, School of Medicine, Shanghai, People's Republic of China.

IUBMB Life
|November 13, 2018
PubMed

Insights

MicroRNA-98 (miR-98) is down-regulated in cardiac ischemia reperfusion injury. Increasing miR-98 levels protects against heart damage and cell death, suggesting its therapeutic potential.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Biochemistry

Background:

  • Cardiovascular ischemic diseases pose significant health risks.
  • MicroRNAs (miRNAs) play a crucial role in regulating cardiac injury.
  • The specific role of miR-98 in cardiac ischemia reperfusion (I/R) injury remains largely unexplored.

Purpose of the Study:

  • To investigate the expression and function of miR-98 in myocardial ischemia reperfusion (I/R) injury.
  • To determine the therapeutic potential of miR-98 in mitigating cardiac I/R damage.

Main Methods:

  • Assessed miR-98 expression in cardiomyocytes subjected to hypoxia/reoxygenation (H/R) and in I/R rat myocardium.
  • Utilized H9c2 cells to study the effects of miR-98 over-expression on H/R injury.
  • Employed bioinformatic analysis (MiRanda, TargetScan) and luciferase assays to identify miR-98 targets.

Main Results:

  • miR-98 expression was significantly down-regulated in both H/R cardiomyocytes and I/R rat myocardium.
  • Over-expression of miR-98 reduced myocardial oxidative stress, ischemic injury, and apoptosis in H/R-treated H9c2 cells.
  • Death-associated protein kinase 1 (DAPK1) was confirmed as a direct target of miR-98.

Conclusions:

  • miR-98 expression is decreased during cardiac ischemia reperfusion injury.
  • miR-98 exhibits protective effects against myocardial I/R injury by reducing oxidative stress and apoptosis.
  • miR-98 presents a potential novel molecular marker and therapeutic target for myocardial I/R injury.

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