microRNA‑3941 targets IGF2 to control LPS‑induced acute pneumonia in A549 cells

Shinuan Fei1, Lichun Cao2, Liangzhi Pan3

  • 1Department of Pediatrics, Edong Healthcare Group, Huangshi Maternity and Children's Health Hospital, Huangshi, Hubei 435000, P.R. China.

Insights

MicroRNA-3941 (miR-3941) is downregulated in childhood acute pneumonia, exacerbating lung injury by targeting insulin-like growth factor 2 (IGF2) and activating the PI3K/AKT pathway. Restoring miR-3941 shows therapeutic potential.

Area of Science:

  • Molecular Biology
  • Immunology
  • Pulmonology

Background:

  • Acute pneumonia is a significant cause of childhood morbidity.
  • Lipopolysaccharides (LPS) trigger inflammatory responses implicated in pneumonia pathogenesis.
  • MicroRNAs (miRNAs) play crucial roles in regulating cellular processes and disease development.

Purpose of the Study:

  • To investigate the role and regulatory mechanism of microRNA-3941 (miR-3941) in lipopolysaccharides (LPS)-induced acute pneumonia.
  • To explore the relationship between miR-3941, insulin-like growth factor 2 (IGF2), and the PI3K/AKT pathway in acute pneumonia.

Main Methods:

  • Detected miR-3941 expression in child patients with acute pneumonia.
  • Established a cellular model of acute pneumonia using LPS-treated A549 cells.
  • Assessed cell viability, apoptosis, inflammation, and the expression of miR-3941, IGF2, and PI3K/AKT pathway components.

Main Results:

  • miR-3941 was significantly downregulated in patients and LPS-treated cells.
  • LPS induced cell injury, apoptosis, and inflammation, accompanied by decreased miR-3941.
  • Overexpression of miR-3941 alleviated LPS-induced injury; IGF2 was identified as a direct target, and its knockdown mimicked miR-3941's protective effects.
  • miR-3941 inhibited PI3K/AKT pathway activation, while IGF2 knockdown reversed this inhibition.

Conclusions:

  • Downregulation of miR-3941 contributes to LPS-induced acute pneumonia by targeting IGF2 and activating the PI3K/AKT pathway.
  • miR-3941 demonstrates potential as a therapeutic target for acute pneumonia in children.

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