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MicroRNA-194 participates in endotoxemia induced myocardial injury via promoting apoptosis

Y Zhai1, N Ding

  • 1Health Management Division, The People's Hospital of Weifang, Weifang, Shandong, China. ddnn-0057@163.com.

European Review for Medical and Pharmacological Sciences
|April 25, 2018
PubMed
Abstract

Insights

MicroRNA-194 expression increases during lipopolysaccharide-induced myocardial injury. This microRNA promotes cardiomyocyte apoptosis by activating the Wnt/β-catenin pathway, contributing to endotoxemia-related heart damage.

Area of Science:

  • Molecular Biology
  • Cardiovascular Research
  • Cell Biology

Background:

  • Lipopolysaccharide (LPS) is a potent endotoxin that can induce myocardial injury.
  • MicroRNAs (miRNAs) play critical roles in regulating cellular processes, including apoptosis and cardiac function.
  • Understanding the specific roles of miRNAs in LPS-induced myocardial injury is crucial for developing therapeutic strategies.

Purpose of the Study:

  • To investigate the expression levels of microRNA-194 in a lipopolysaccharide (LPS)-induced myocardial injury model.
  • To elucidate the underlying molecular mechanisms by which microRNA-194 influences cardiomyocyte apoptosis and myocardial injury.

Main Methods:

  • Establishment of an LPS-induced H9c2 cardiomyocyte injury model.
  • Detection of microRNA-194 expression levels using quantitative real-time PCR (qRT-PCR).
  • Assessment of cardiomyocyte survival and apoptosis following microRNA-194 manipulation (overexpression and knockdown).
  • Bioinformatic prediction and experimental validation (dual luciferase reporter assay, Western blot) of microRNA-194 target genes.
  • Investigation of the Wnt/β-catenin signaling pathway using qRT-PCR and Western blot.

Main Results:

  • MicroRNA-194 expression was significantly upregulated in LPS-treated H9c2 cells in a time-dependent manner.
  • Overexpression of microRNA-194 directly targeted and inhibited the expression of Slc7a5.
  • Transfection with microRNA-194 mimics promoted H9c2 cell apoptosis, an effect reversed by co-expression of Slc7a5.
  • MicroRNA-194 was found to activate the Wnt/β-catenin signaling pathway, contributing to cardiomyocyte apoptosis.

Conclusions:

  • MicroRNA-194 plays a pro-apoptotic role in cardiomyocytes during LPS-induced myocardial injury.
  • The mechanism involves the direct inhibition of Slc7a5 and activation of the Wnt/β-catenin pathway.
  • MicroRNA-194 is a key mediator in endotoxemia-induced myocardial damage, highlighting its potential as a therapeutic target.

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