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MicroRNA-182-5p aggravates ulcerative colitis by inactivating the Wnt/β-catenin signaling pathway through

Yan Xu1, Junwen Yang2, Xiaoli Chen2

  • 1Department of Health Management Center, Xiangya Hospital, Central South University, Changsha, Hunan 410008, PR China.

Genomics
|April 4, 2022
PubMed

Insights

MicroRNA-182-5p aggravates ulcerative colitis (UC) by inhibiting the Wnt/β-catenin pathway. This involves targeting DNMT3A to upregulate SMARCA5, worsening intestinal barrier dysfunction in UC models.

Area of Science:

  • Gastroenterology
  • Molecular Biology
  • Immunology

Background:

  • Ulcerative colitis (UC) is a chronic inflammatory bowel disease with complex molecular underpinnings.
  • MicroRNAs (miRNAs) play crucial roles in regulating cellular processes relevant to inflammation and tissue repair.
  • Dysregulation of specific miRNAs, like miR-182-5p, may contribute to UC pathogenesis.

Purpose of the Study:

  • To elucidate the novel molecular mechanisms of microRNA (miR)-182-5p in ulcerative colitis (UC).
  • To investigate the role of miR-182-5p, SMARCA5, and the Wnt/β-catenin signaling pathway in UC.
  • To determine how miR-182-5p influences intestinal barrier function and inflammation in UC models.

Main Methods:

  • Analysis of colon tissues from UC patients.
  • Generation of dextrose sodium sulfate (DSS)-induced mouse models and interleukin-1β (IL-1β)-induced Caco-2 cell models.
  • Manipulation of miR-182-5p, SMARCA5, and Wnt/β-catenin signaling in cellular and animal models to assess functional impacts.

Main Results:

  • MiR-182-5p and SMARCA5 were upregulated, while DNMT3A, β-catenin, and Cyclin D1 were downregulated in UC patients, IL-1β-stimulated Caco-2 cells, and DSS-treated mice.
  • MiR-182-5p targets DNMT3A, leading to SMARCA5 upregulation and subsequent Wnt/β-catenin pathway inhibition.
  • SMARCA5 silencing or Wnt/β-catenin pathway activation improved Caco-2 cell function and ameliorated intestinal barrier dysfunction in DSS-treated mice.

Conclusions:

  • MiR-182-5p exacerbates UC by inactivating the Wnt/β-catenin signaling pathway.
  • This inactivation occurs through DNMT3A-mediated SMARCA5 methylation, impacting intestinal barrier integrity.
  • Targeting the miR-182-5p/DNMT3A/SMARCA5 axis presents a potential therapeutic strategy for UC.
Keywords:
ApoptosisDNA methyltransferase 3AEpithelial barrier functionIntestinal barrier dysfunctionMethylationMicroRNA-182-5pProliferationSMARCA5Ulcerative colitisWnt/β-catenin signaling pathway

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