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Related Concept Videos

Inflammatory Bowel Disease II: Ulcerative Colitis01:20

Inflammatory Bowel Disease II: Ulcerative Colitis

Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal BarrierA...
Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
Renewal of Intestinal Stem Cells01:23

Renewal of Intestinal Stem Cells

The intestinal epithelial lining rapidly renews every 4 to 5 days. The renewal is facilitated by intestinal stem cells (ISCs) located at the base of the crypt– a gland located at the bottom of each villus. ISCs divide asymmetrically to form new stem cells and progenitor daughter cells. The daughter cells are called transit-amplifying (TA) cells which move upwards along the crypt and either differentiate into absorptive cells– the enterocytes or secretory cells– including the goblet,...
Inflammatory Bowel Disease I: Ulcerative Colitis01:27

Inflammatory Bowel Disease I: Ulcerative Colitis

Introduction
Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
Risk Factors
The exact cause of IBD remains unclear, although it is believed to be due to a mix of genetic, environmental, microbial, and immune factors. Genetic factors are significant in determining susceptibility to IBD, with family history being a critical risk factor. Individuals with a first-degree relative who has IBD are at...

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Related Experiment Video

Updated: May 22, 2026

Analyzing Beneficial Effects of Nutritional Supplements on Intestinal Epithelial Barrier Functions During Experimental Colitis
08:58

Analyzing Beneficial Effects of Nutritional Supplements on Intestinal Epithelial Barrier Functions During Experimental Colitis

Published on: January 5, 2017

Bin1 attenuation suppresses experimental colitis by enforcing intestinal barrier function.

Mee Young Chang1, Janette Boulden, M Carmen Valenzano

  • 1Lankenau Institute for Medical Research, Wynnewood, PA 19096, USA.

Digestive Diseases and Sciences
|April 25, 2012
PubMed
Summary
This summary is machine-generated.

Bin1 gene attenuation protected against experimental colitis, particularly in females, by improving intestinal barrier function. This suggests Bin1 is a potential therapeutic target for inflammatory bowel disease (IBD).

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Related Experiment Videos

Last Updated: May 22, 2026

Analyzing Beneficial Effects of Nutritional Supplements on Intestinal Epithelial Barrier Functions During Experimental Colitis
08:58

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Published on: January 5, 2017

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Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice
07:34

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice

Published on: December 16, 2021

Area of Science:

  • Gastroenterology
  • Molecular Biology
  • Immunology

Background:

  • Inflammatory bowel disease (IBD) is linked to compromised intestinal barriers and defective cellular tight junctions.
  • Targeting genes to enhance tight junction function offers potential therapeutic strategies for IBD.

Purpose of the Study:

  • To investigate the role of the tumor suppressor gene Bin1 in modulating the severity of experimental colitis.
  • To evaluate Bin1 as a potential therapeutic target for IBD.

Main Methods:

  • Ablation of the Bin1 gene in a mosaic mouse model to assess its impact on experimental colitis and intestinal barrier function.
  • Characterization of pathology, histology, cytokine expression, and ex vivo physiological measurements of barrier function.

Main Results:

  • Bin1 gene attenuation reduced experimental colitis severity, with a more pronounced protective effect observed in female mice.
  • This protection correlated with increased transepithelial electrical resistance (TER) and reduced paracellular flux, indicating improved barrier function.
  • Bin1 attenuation did not impact short-circuit current or the epithelial barrier's response to non-inflammatory permeability enhancers.

Conclusions:

  • Bin1 acts as a genetic modifier of experimental colitis by influencing the paracellular pathway regulated by cellular tight junctions.
  • These findings provide preclinical evidence supporting Bin1 as a novel therapeutic target for treating IBD.