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MicroRNA‑451 protects against cardiomyocyte anoxia/reoxygenation injury by inhibiting high mobility group box 1

Jing Xie1, Xiaorong Hu1, Chunfeng Yi1

  • 1Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei 430060, P.R. China.

Molecular Medicine Reports
|April 29, 2016
PubMed

Insights

MicroRNA-451 (miR-451) protects heart cells from damage during anoxia/reoxygenation (A/R) injury. Upregulating miR-451 reduces High mobility group box 1 (HMGB1) expression, mitigating cardiac A/R injury.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Biochemistry

Background:

  • High mobility group box 1 (HMGB1) protein is implicated in myocardial ischemia/reperfusion (I/R) injury.
  • MicroRNAs (miRNAs) are key regulators in cardiac I/R injury pathways.

Purpose of the Study:

  • To investigate the protective role of miR-451 against cardiomyocyte anoxia/reoxygenation (A/R) injury.
  • To determine if miR-451 attenuates HMGB1 expression in cardiac A/R injury.

Main Methods:

  • Neonatal rat ventricular cardiomyocytes subjected to A/R injury.
  • Assessed cell viability, apoptosis, superoxide dismutase (SOD) activity, and cleaved-caspase-3 expression.
  • Utilized a luciferase assay to confirm direct targeting of HMGB1 by miR-451.

Main Results:

  • miR-451 expression decreased during A/R; upregulation enhanced cell viability and SOD activity.
  • Upregulation of miR-451 significantly reduced cardiomyocyte apoptosis and HMGB1 expression (mRNA and protein).
  • Luciferase assay confirmed HMGB1 mRNA as a direct target of miR-451.

Conclusions:

  • Upregulation of miR-451 confers protection against A/R-induced cardiomyocyte injury.
  • miR-451 exerts its protective effects by inhibiting HMGB1 expression.
  • miR-451 represents a potential therapeutic target for managing cardiac A/R injury.

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