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Long noncoding RNA MAPKAPK5-AS1 promoted lipopolysaccharide-induced inflammatory damage in the myocardium by sponging

Weiwei Chen1,2, Guangyuan Gao1,2, Mengjie Yan1,2

  • 1Department of Cardiology, China-Japan Union Hospital of Jilin University, Changchun City, 130033, Jilin Province, People's Republic of China.

Molecular Medicine (Cambridge, Mass.)
|October 20, 2021
PubMed
Abstract

Insights

Sepsis-induced myocardial dysfunction involves long non-coding RNA MAPKAPK5-AS1. This study reveals MAPKAPK5-AS1 promotes inflammation and apoptosis via the miR-124-3p/E2F3 axis, offering therapeutic targets for sepsis.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Sepsis-induced myocardial dysfunction (SIMD) is a critical condition with high mortality.
  • Understanding the molecular mechanisms underlying SIMD is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the role and mechanism of long non-coding RNA MAPKAPK5-AS1 (lncRNA MAPKAPK5-AS1) in lipopolysaccharide (LPS)-induced inflammation and myocardial dysfunction.
  • To elucidate the regulatory pathway involving lncRNA MAPKAPK5-AS1, miR-124-3p, and E2F3 in the context of sepsis.

Main Methods:

  • In vivo studies using male Sprague-Dawley rats and in vitro studies using rat cardiomyocytes (H9C2 cells).
  • Assessment of inflammation and apoptosis using Western blotting, RT-PCR, TUNEL assay, and flow cytometry.
  • Investigation of the interaction between lncRNA MAPKAPK5-AS1 and miR-124-3p, and the target of miR-124-3p (E2F3).

Main Results:

  • LPS challenge increased MAPKAPK5-AS1 expression and decreased miR-124-3p expression in vivo and in vitro.
  • Knockdown of MAPKAPK5-AS1 attenuated LPS-induced cardiomyocyte apoptosis and inflammation.
  • MAPKAPK5-AS1 was found to negatively regulate miR-124-3p, which in turn downregulated E2F3 expression, establishing the MAPKAPK5-AS1/miR-124-3p/E2F3 regulatory axis.

Conclusions:

  • The MAPKAPK5-AS1/miR-124-3p/E2F3 axis plays a significant role in regulating cardiomyocyte apoptosis and inflammatory responses induced by LPS.
  • Targeting the MAPKAPK5-AS1/miR-124-3p/E2F3 pathway may offer a novel therapeutic strategy for sepsis-induced myocardial dysfunction.
Keywords:
E2F3Inflammatory responseLipopolysaccharideMAPKAPK5-AS1microRNA-124-3p

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