circVMA21 combining with TAF15 stabilizes SOCS3 mRNA to relieve septic lung injury through regulating NF-κB

Zi-Gui Zhu1, Gu-Qing Liao1, Jian-Xin Zhang2

  • 1Department of Intensive Care Unit, The Affiliated Nanhua Hospital, Hengyang Medical College, University of South China, Hengyang 421002, Hunan Province, PR China.

Molecular Immunology
|September 26, 2022
PubMed
Abstract

Insights

Circular RNA VMA21 (CircVMA21) protects against sepsis-induced lung injury by regulating the TAF15/SOCS3/NF-κB pathway. This study clarifies the molecular mechanism of CircVMA21 in mitigating inflammation and oxidative stress.

Area of Science:

  • Biomedical Science
  • Molecular Biology
  • Sepsis Research

Background:

  • Sepsis-induced lung injury poses significant health risks.
  • Circular RNA VMA21 (CircVMA21) shows anti-inflammatory potential, but its mechanism is unclear.

Purpose of the Study:

  • To elucidate the molecular mechanism of CircVMA21 in sepsis-induced lung injury.
  • To investigate the role of CircVMA21 in regulating inflammatory responses and oxidative stress.

Main Methods:

  • Established sepsis-induced lung injury models in mice and WI-38 cells using lipopolysaccharide (LPS).
  • Assessed lung injury, apoptosis, inflammatory cytokines, oxidative stress markers, and protein expression.
  • Utilized RT-qPCR, ELISA, western blot, RIP, and RNA-pull down assays to analyze molecular interactions and expression levels.

Main Results:

  • CircVMA21 and SOCS3 expression were downregulated in LPS-induced lung injury.
  • Overexpression of CircVMA21 or SOCS3 alleviated LPS-induced injury by reducing inflammation, oxidative stress, and apoptosis.
  • CircVMA21 stabilized SOCS3 mRNA via TAF15, inactivating the NF-κB pathway.

Conclusions:

  • CircVMA21 mitigates sepsis-induced lung injury by suppressing inflammation, oxidative stress, and apoptosis.
  • The protective effect is mediated through the TAF15/SOCS3/NF-κB signaling axis.

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