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MicroRNA-214-3p Ameliorates LPS-Induced Cardiomyocyte Injury by Inhibiting Cathepsin B.

W Yan1, Y Feng1, Z Lei1

  • 1The First Affiliated Hospital, Department of Cardiovascular Surgery, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China.

Folia Biologica
|November 17, 2022
PubMed
Summary
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MicroRNA miR-214-3p protects against sepsis-induced myocardial injury by targeting cathepsin B (CTSB). This study reveals miR-214-3p inhibits cardiomyocyte damage, offering new therapeutic strategies for sepsis complications.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Cell Biology

Background:

  • Myocardial injury is a frequent sepsis complication.
  • The protective role of microRNA (miRNA) miR-214-3p in sepsis-induced myocardial injury is established, but its precise mechanism remains unclear.
  • Lipopolysaccharide (LPS) is a key component in inducing sepsis-related cellular damage.

Purpose of the Study:

  • To elucidate the mechanism by which miR-214-3p exerts its protective effects against LPS-induced cardiomyocyte injury.
  • To investigate the potential interaction between miR-214-3p and cathepsin B (CTSB) in the context of myocardial injury.

Main Methods:

  • AC16 cells were treated with LPS to establish a cardiomyocyte injury model.
  • Cell viability, apoptosis, and levels of key proteins (caspase-3, Bax, Bcl-2, ANP, BNP, Myh6, Myh7) and oxidative stress markers (ROS, MDA, SOD) were assessed.

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  • Expression levels of miR-214-3p and CTSB were analyzed, and their regulatory relationship was investigated using miR-214-3p mimics, inhibitors, and CTSB silencing.

    • Main Results:

    • LPS treatment decreased AC16 cell viability and increased apoptosis, alongside elevated caspase-3, Bax, ROS, MDA, ANP, BNP, Myh6, and Myh7, while decreasing Bcl-2 and SOD.
    • miR-214-3p was downregulated, and CTSB was upregulated in LPS-treated cells, with miR-214-3p directly targeting and reducing CTSB expression.
    • Overexpression of miR-214-3p or silencing of CTSB significantly attenuated LPS-induced apoptosis and oxidative stress, restoring cellular protective mechanisms. CTSB silencing also reduced cardiac marker expression, effects reversed by miR-214-3p inhibition.

    Conclusions:

    • miR-214-3p plays a critical protective role in mitigating LPS-induced myocardial injury by targeting and downregulating CTSB.
    • This molecular pathway involving miR-214-3p and CTSB offers a novel therapeutic target for managing sepsis-associated myocardial damage.