Long noncoding RNA XIST regulates cardiomyocyte apoptosis by targeting miR-873-5p/MCL1 axis

C-L Cai1, L Jin, X-L Lang

  • 1Department of Cardiovascular Surgery, Shanghai Changhai Hospital, The Second Military Medical University, Shanghai, China. caicl1000@alu.fudan.edu.cn.

Abstract

Insights

Downregulation of miR-873-5p protects against myocardial infarction (MI) apoptosis. Long non-coding RNA XIST (lncRNA XIST) inhibits apoptosis, and its inhibition upregulates miR-873-5p, impacting cardiomyocyte apoptosis.

Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • Cellular Biology

Background:

  • Myocardial infarction (MI) is a leading cause of mortality.
  • Understanding the molecular mechanisms regulating cardiomyocyte apoptosis is crucial for developing effective therapies.
  • MicroRNAs (miRNAs) and long non-coding RNAs (lncRNAs) play significant roles in cardiovascular diseases.

Purpose of the Study:

  • To investigate the expression of miR-873-5p and lncRNA XIST in myocardial infarction.
  • To elucidate the interaction mechanism between miR-873-5p and lncRNA XIST.
  • To determine the effect of their interaction on MCL1 expression and cardiomyocyte apoptosis.

Main Methods:

  • Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) for gene expression analysis.
  • Western blot to assess protein levels.
  • Experiments in H9c2 cells under hypoxic conditions to mimic MI.
  • In vivo studies using myocardial infarction rat models.

Main Results:

  • miR-873-5p was downregulated in myocardial infarction tissues.
  • lncRNA XIST expression was upregulated in myocardial infarction tissues and inhibited apoptosis in H9c2 cells.
  • Inhibition of lncRNA XIST led to increased miR-873-5p expression and MCL1 downregulation, subsequently increasing apoptosis.
  • A significant correlation was observed between miR-873-5p and lncRNA XIST expression.

Conclusions:

  • lncRNA XIST plays a critical role in regulating cardiomyocyte apoptosis.
  • The lncRNA XIST/miR-873-5p axis influences cardiomyocyte apoptosis by targeting MCL1.
  • Targeting the lncRNA XIST/miR-873-5p pathway may offer a therapeutic strategy for myocardial infarction.

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