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Lipopolysaccharide Inhibits Alpha Epithelial Sodium Channel Expression via MiR-124-5p in Alveolar Type 2  Epithelial

Yan Ding1, Yong Cui2, Zhiyu Zhou1

  • 1Department of Stem Cells and Regenerative Medicine, College of Basic Medical Science, China Medical University, Shenyang 110122, China.

Biomed Research International
|March 20, 2020
PubMed

Insights

Mesenchymal stem cells-conditioned medium (MSCs-CM) may treat lung injury by reducing miR-124-5p, which lowers epithelial sodium channel (ENaC) expression and function. This study reveals miR-124-5p as a potential therapeutic target for acute lung injury.

Area of Science:

  • Biomedical research
  • Molecular biology
  • Pulmonary medicine

Background:

  • Mesenchymal stem cells-conditioned medium (MSCs-CM) shows promise for pulmonary diseases.
  • Mechanisms of MSCs-CM involving microRNAs in lung ion transport are not well understood.
  • Acute lung injury involves epithelial sodium channel (ENaC) dysfunction.

Purpose of the Study:

  • Investigate the role of miR-124-5p in lipopolysaccharide-induced ENaC dysfunction.
  • Identify the molecular targets of miR-124-5p in alveolar epithelial cells.
  • Explore the therapeutic potential of targeting miR-124-5p in acute lung injury.

Main Methods:

  • Quantitative analysis of miR-124-5p expression after MSCs-CM administration.
  • Manipulation of miR-124-5p levels in mouse alveolar type 2 epithelial (AT2) cells.
  • Dual luciferase and Ussing chamber assays to confirm target interaction and functional impact.

Main Results:

  • MSCs-CM administration led to decreased miR-124-5p expression.
  • miR-124-5p directly targets the 3'-untranslated region of α-ENaC.
  • miR-124-5p inhibition of α-ENaC expression and amiloride-sensitive currents was confirmed.

Conclusions:

  • miR-124-5p regulates α-ENaC expression and function in alveolar epithelial cells.
  • Downregulation of miR-124-5p by MSCs-CM may contribute to its protective effects in acute lung injury.
  • Targeting miR-124-5p offers a potential therapeutic strategy for acute lung injury.

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