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Related Experiment Video

Updated: Jan 7, 2026

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ST3Gal1 modulates intestinal barrier function and impacts human ulcerative colitis.

Yin Tian1, Yun Liu2, Yangyang Shang2

  • 1Department of Gastroenterology, The People's Hospital of Yubei District of Chongqing City, Chongqing 401120, P.R. China.

Molecular Medicine Reports
|December 19, 2025
PubMed
Summary

ST3Gal1 protein regulates intestinal barrier function. Suppressing ST3Gal1 enhances barrier integrity, while overexpression deteriorates it, impacting inflammatory bowel disease pathogenesis.

Keywords:
ST3Gal1barrierinflammationsialylationtriple culture model

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Area of Science:

  • Gastroenterology
  • Cell Biology
  • Biochemistry

Background:

  • Inflammatory bowel disease (IBD) pathogenesis involves intestinal mucosal barrier dysfunction.
  • Protein sialylation is crucial for maintaining intestinal barrier integrity.
  • The role of ST3Gal1-mediated α2,3-sialylation in IBD remains to be fully elucidated.

Purpose of the Study:

  • To investigate the impact of ST3Gal1-catalyzed α2,3-sialylation on intestinal barrier function.
  • To explore the role of ST3Gal1 in the pathogenesis of ulcerative colitis (UC).

Main Methods:

  • Established an in vitro triple-culture model simulating healthy and inflamed human intestinal states.
  • Utilized adenoviral and lentiviral vectors for ST3Gal1 knockdown and overexpression in intestinal epithelial cells (IECs).
  • Assessed intestinal barrier function using trans-epithelial electrical resistance and FITC-dextran permeability assays.

Main Results:

  • ST3Gal1 expression correlated with intestinal inflammation in UC patients and a colitis mouse model.
  • Suppressed ST3Gal1 expression enhanced intestinal barrier function; overexpression deteriorated it.
  • ST3Gal1 modulated expression of MUC2, TFF3, CDX2, p-STAT3, IL-1β, IL-6, and IL-8, influencing barrier integrity and inflammation.

Conclusions:

  • ST3Gal1 plays a significant role in regulating intestinal barrier function.
  • ST3Gal1-catalyzed α2,3-sialylation impacts UC pathogenesis by affecting barrier-associated proteins and inflammatory mediators.
  • Targeting ST3Gal1 may offer therapeutic potential for inflammatory bowel diseases.