miR-942-5p prevents sepsis-induced acute lung injury via targeting TRIM37

Qiang Lu1, Dinggao Zhang1, Hui Liu1

  • 1Department of Emergency, Yiyang Central Hospital, Yiyang, China.

Insights

MicroRNAs (miRNAs) like miR-942-5p protect lung cells from injury caused by lipopolysaccharide (LPS). This protective effect involves reducing apoptosis and inflammation by targeting TRIM37 expression.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Immunology

Background:

  • MicroRNAs (miRNAs) are key regulators in sepsis-induced acute lung injury (ALI).
  • Understanding specific miRNA roles, like miR-942-5p, is crucial for developing therapeutic strategies against ALI.
  • Lipopolysaccharide (LPS) is a common trigger for ALI models.

Purpose of the Study:

  • To investigate the role and mechanism of miR-942-5p in lipopolysaccharide (LPS)-induced A549 cell injury.
  • To determine if miR-942-5p affects apoptosis and inflammation in an ALI model.
  • To identify the downstream target of miR-942-5p involved in LPS-induced cell damage.

Main Methods:

  • Cell viability assessed by CCK-8 assay, apoptosis by flow cytometry, and inflammatory cytokines by ELISA.
  • Expression levels of miR-942-5p and TRIM37 measured using real-time PCR and Western blot.
  • miRNA-target interaction validated through bioinformatics, luciferase reporter assays, and RNA pull-down assays.

Main Results:

  • LPS treatment decreased miR-942-5p expression in A549 cells, suppressed cell viability, increased apoptosis, and elevated inflammatory cytokine levels.
  • Overexpression of miR-942-5p counteracted LPS-induced effects, enhancing cell viability and reducing apoptosis and inflammation.
  • miR-942-5p was confirmed to directly target TRIM37, and TRIM37 upregulation reversed the protective effects of miR-942-5p.

Conclusions:

  • miR-942-5p plays a protective role against LPS-induced A549 cell injury.
  • The mechanism involves miR-942-5p inhibiting apoptosis and inflammation by negatively regulating TRIM37.
  • miR-942-5p represents a potential therapeutic target for sepsis-induced acute lung injury.

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