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YTHDC1 inhibits autophagy-dependent NF-κB signaling by stabilizing Beclin1 mRNA in macrophages

Li Zhou1, Ling Zhang1, Yan Lv1

  • 1Center for Translational Medicine, The Affiliated Zhangjiagang Hospital of Soochow University, No. 68 West Jiyang Road, Suzhou, 215600, China.

Journal of Inflammation (London, England)
|June 14, 2024
PubMed
Abstract

Insights

YTHDC1 protein suppresses inflammation in inflammatory bowel disease (IBD) by stabilizing Beclin1 mRNA, enhancing autophagy, and inhibiting NF-κB signaling. This finding highlights YTHDC1 as a potential therapeutic target for IBD treatment.

Area of Science:

  • Immunology
  • Molecular Biology
  • Gastroenterology

Background:

  • YTHDC1 is a key nuclear reader of m(6)A RNA modifications, regulating mRNA processes.
  • Its role and regulatory mechanisms in inflammatory bowel disease (IBD) are not well understood.

Purpose of the Study:

  • To investigate the functional role of YTHDC1 in inflammatory responses.
  • To explore the underlying molecular mechanisms of YTHDC1 in the context of IBD.

Main Methods:

  • Established dextran sulfate sodium (DSS)-induced colitis and LPS/IFN-γ-stimulated macrophage models.
  • Assessed YTHDC1 expression, utilized lentiviral vectors for overexpression/inhibition, and employed NF-κB inhibitor JSH-23.
  • Investigated YTHDC1 interaction with Beclin1 mRNA using RIP and confirmed m6A modification via MeRIP.

Main Results:

  • YTHDC1 expression was significantly downregulated in colitis and stimulated macrophages.
  • YTHDC1 overexpression reduced pro-inflammatory markers (iNOS, CD86, IL-6) and NF-κB activation.
  • YTHDC1 stabilized Beclin1 mRNA, enhancing autophagy and inhibiting NF-κB signaling.

Conclusions:

  • YTHDC1 suppresses macrophage-mediated inflammation by stabilizing Beclin1 mRNA and promoting autophagy.
  • YTHDC1 represents a potential therapeutic target for inflammatory bowel disease.
Keywords:
AutophagyBeclin1IBDInflammationNF-κBYTHDC1

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