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Influence of lncRNA MALAT1 on septic lung injury in mice through p38 MAPK/p65 NF-κB pathway

L-P Lin1, G-H Niu, X-Q Zhang

  • 1Department of Obstetrics and Gynecology, Xiamen Maternal and Child Health Hospital, Xiamen, China. wind459@126.com.

European Review for Medical and Pharmacological Sciences
|February 20, 2019
PubMed
Abstract

Insights

Knocking down long non-coding RNA MALAT1 significantly improves septic lung injury in mice. This occurs by inhibiting the p38 MAPK/p65 NF-κB signaling pathway, offering potential therapeutic insights.

Area of Science:

  • Molecular Biology
  • Immunology
  • Pathology

Background:

  • Sepsis-induced lung injury is a critical complication with limited treatment options.
  • Long non-coding RNAs (lncRNAs) play emerging roles in inflammatory diseases.
  • Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is implicated in various pathologies.

Purpose of the Study:

  • To investigate the role of lncRNA MALAT1 in a mouse model of septic lung injury.
  • To elucidate the underlying molecular mechanisms involving the p38 MAPK/p65 NF-κB signaling pathway.
  • To provide a basis for future clinical interventions against septic lung injury.

Main Methods:

  • Establishment of a lipopolysaccharide (LPS)-induced septic lung injury model in C57 mice.
  • Knockdown of MALAT1 using small interfering RNA (siRNA).
  • Assessment of lung injury markers (wet/dry weight, MPO activity), inflammatory cell infiltration (BALF), cytokine expression (RT-PCR), and signaling pathway activation (Western blotting, immunohistochemistry).

Main Results:

  • MALAT1 expression was significantly upregulated in septic lung injury.
  • MALAT1 knockdown ameliorated lung pathological damage and reduced lung wet/dry ratio.
  • Inflammatory cell infiltration and pro-inflammatory cytokine levels (TNF-α, IL-1, IL-6) were significantly decreased post-MALAT1 knockdown.
  • Inhibition of MALAT1 suppressed LPS-induced upregulation of p38 and deactivated the p38 MAPK/p65 NF-κB pathway.

Conclusions:

  • lncRNA MALAT1 knockdown effectively mitigates septic lung injury in mice.
  • The protective effect is mediated through the inhibition of the p38 MAPK/p65 NF-κB signaling pathway.
  • Targeting MALAT1 presents a potential therapeutic strategy for septic lung injury.

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