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SHANK3 Regulates Intestinal Barrier Function Through Modulating ZO-1 Expression Through the PKCε-dependent Pathway.

Shu-Chen Wei1, Hsin-Fang Yang-Yen, Po-Nien Tsao

  • 1*Department of Internal Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan; †Institutes of Molecular Biology, Academia Sinica, Taipei, Taiwan; ‡Department of Pediatrics, College of Medicine, National Taiwan University, Taipei, Taiwan; §Department of Internal Medicine, Far Eastern Memorial Hospital, New Taipei, Taiwan; ‖Department of Integrated Diagnostics and Therapeutics, College of Medicine, National Taiwan University, Taipei, Taiwan; ¶Graduate Institute of Physiology, College of Medicine, National Taiwan University, Taipei, Taiwan; **Bioinformatics and Biostatistics Core, Center of Genomic Medicine, National Taiwan University, Taipei, Taiwan; ††Graduate Institute of Biomedical Electronics and Bioinformatics, National Taiwan University, Taipei, Taiwan; ‡‡Department of Pathology and Forensic Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan; §§Gastrointestinal Unit and Center for the Study of Inflammatory Bowel Disease, Massachusetts General Hospital, Boston, Massachusetts; ‖‖UT Southwestern Medical Center, Dallas, Texas; and ¶¶Institutes of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.

Inflammatory Bowel Diseases
|September 15, 2017
PubMed
Summary
This summary is machine-generated.

SHANK3 protein levels impact gut barrier integrity. Lower SHANK3 expression leads to a leaky gut barrier, offering new insights into inflammatory bowel disease and Crohn's disease treatment.

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Area of Science:

  • Gastroenterology
  • Cell Biology
  • Neuroscience

Background:

  • Gut barrier integrity is compromised in inflammatory bowel disease (IBD), but mechanisms are unclear.
  • SHANK3 mutations link autism to increased IBD risk.
  • This study investigates SHANK3's role in IBD pathogenesis.

Purpose of the Study:

  • To explore the role of SHANK3 in inflammatory bowel disease (IBD).
  • To investigate the in vivo and in vitro mechanisms by which SHANK3 influences gut barrier function.
  • To determine the correlation between SHANK3 expression and gut barrier markers in Crohn's disease patients.

Main Methods:

  • Induced dextran sulfate sodium (DSS) colitis in SHANK3 knockout mice.
  • Assessed epithelial barrier function using transepithelial electrical resistance (TER), paracellular permeability, and Salmonella invasion assays.
  • Analyzed tight junction protein expression (ZO-1), kinase activity, and SHANK3 expression in mouse models and human Crohn's disease tissue.

Main Results:

  • SHANK3 knockout mice showed increased susceptibility to DSS colitis and impaired epithelial barrier function.
  • SHANK3 deficiency decreased ZO-1 expression via a PKCε-dependent pathway, leading to a 'leaky gut' phenotype.
  • SHANK3 expression positively correlated with ZO-1 and PKCε in Crohn's disease colonic tissues.

Conclusions:

  • SHANK3 expression levels directly influence ZO-1 expression and intestinal epithelial barrier function.
  • SHANK3 plays a critical role in maintaining gut barrier integrity.
  • Findings suggest SHANK3 as a potential therapeutic target for Crohn's disease.