Methylprednisolone Attenuates Lipopolysaccharide-Induced Sepsis by Modulating the Small Nucleolar RNA Host Gene

Li Zhang1, Wei Tan1, Xinmiao Song1

  • 1Department of Respiratory and Critical Care Medicine, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.

DNA and Cell Biology
|November 12, 2021
PubMed

Insights

Methylprednisolone succinate (MP) treats sepsis by regulating the SNHG5/CPNE1 pathway. This study reveals MP

Area of Science:

  • Biomedical Research
  • Molecular Biology
  • Immunology

Background:

  • Sepsis is a critical global health issue.
  • Methylprednisolone sodium succinate (MP) is used to manage inflammation.
  • The precise mechanism of MP in sepsis requires elucidation.

Purpose of the Study:

  • To investigate the mechanism of MP in sepsis.
  • To explore the role of SNHG5 and CPNE1 in MP's action.
  • To identify potential diagnostic and therapeutic targets for sepsis.

Main Methods:

  • In vitro studies using alveolar type II epithelial cells (ATII cells) exposed to lipopolysaccharide (LPS).
  • Analysis of gene expression (SNHG5, CPNE1) and protein levels (TNF-α, IL-17).
  • In vivo studies using an LPS-induced sepsis mouse model.

Main Results:

  • MP inhibited LPS-induced TNF-α and IL-17 production and suppressed cell growth in ATII cells.
  • MP restored LPS-induced downregulation of SNHG5 expression.
  • The SNHG5/CPNE1 pathway was identified as crucial for MP's therapeutic effect in sepsis.

Conclusions:

  • MP exerts its anti-sepsis effects through the SNHG5/CPNE1 pathway.
  • SNHG5 enhances CPNE1 expression by stabilizing its mRNA.
  • The SNHG5/CPNE1 pathway represents a potential therapeutic target for sepsis treatment.

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