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MiRNA-26a inhibits myocardial infarction-induced apoptosis by targeting PTEN via JAK/STAT pathways

Jianzhong Wang1, Qilong Feng2, Dongke Liang3

  • 1Intersive Care Unit, Shanxi Cardiovascular Hospital, Taiyuan, Shanxi 030024, China.

Cells & Development
|May 17, 2021
PubMed

Insights

MicroRNA-26a (miR-26a) protects heart cells from damage after myocardial infarction (MI). Upregulating miR-26a reduces cell death and improves cardiac function by targeting PTEN.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Biochemistry

Background:

  • Acute myocardial infarction (MI) is a leading global cause of mortality.
  • Mechanisms underlying MI-induced injury remain incompletely understood.
  • The role of microRNAs in cardiac injury requires further investigation.

Purpose of the Study:

  • To investigate the role of microRNA-26a (miR-26a) in myocardial infarction (MI).
  • To elucidate the molecular mechanisms by which miR-26a influences cardiac injury.

Main Methods:

  • Assessed miR-26a and PTEN expression in H2O2-treated cardiomyocytes and MI mouse models.
  • Evaluated cell viability, apoptosis, and cardiac function using MTT assays, BrdU staining, TUNEL assays, flow cytometry, and in vivo agomiR-26a treatment.
  • Investigated the interaction between miR-26a and PTEN using 3'-UTR binding assays.

Main Results:

  • miR-26a expression was decreased, while PTEN was upregulated in conditions of oxidative stress and MI.
  • miR-26a overexpression enhanced cardiomyocyte viability and suppressed apoptosis.
  • miR-26a directly targeted PTEN, modulating PI3K/Akt and JAK/STAT signaling pathways.
  • AgomiR-26a treatment reduced infarct size and improved cardiac function in a mouse model of MI.

Conclusions:

  • miR-26a is downregulated in myocardial infarction and protects against cell death.
  • miR-26a exerts protective effects by targeting PTEN and modulating key signaling pathways.
  • Therapeutic strategies aimed at increasing miR-26a may offer a novel approach for treating MI.
Abstract

Keywords:
JAK/STATMicroRNA-26a-5pMyocardial infarctionPI3K/AktPTEN

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