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Renewal of Intestinal Stem Cells01:23

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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...
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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.
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Related Experiment Video

Updated: Mar 16, 2026

Author Spotlight: Studying the Epithelial Effects of Intestinal Inflammation In Vitro on Established Murine Colonoids
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Alpha-Defensin 5 Expression is Regulated by microRNAs in the Caco-2 Intestinal Epithelial Cell Line.

Donald R B Miles1, Jun Shen2, Alice Y Chuang2

  • 1Johns Hopkins School of Medicine, USA.

Journal of Inflammatory Bowel Diseases & Disorders
|August 16, 2016
PubMed
Summary

MicroRNAs (miRNAs) like miR-124 and miR-924 regulate alpha-defensin 5 (DEFA5) expression. This finding suggests miRNAs play a role in inflammatory bowel disease (IBD) pathogenesis.

Keywords:
DefensinInflammatory bowel diseaseMicroRNA regulation

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Area of Science:

  • Molecular Biology
  • Immunology
  • Gastroenterology

Background:

  • Inflammatory bowel disease (IBD) involves chronic mucosal inflammation due to inappropriate immune responses.
  • Dysregulation of antimicrobial peptides like defensins may contribute to IBD.
  • Alpha-defensin 5 (DEFA5) is an antimicrobial peptide implicated in IBD.

Purpose of the Study:

  • To investigate the role of microRNAs (miRNAs) in regulating DEFA5 expression.
  • To determine if miRNAs contribute to the pathogenesis of IBD.

Main Methods:

  • DEFA5 mRNA and protein expression was induced and measured in Caco-2 cells.
  • Bioinformatic analysis identified potential miRNA binding sites on DEFA5.
  • Luciferase assays and miRNA mimic transfections were used to assess miRNA regulation of DEFA5.

Main Results:

  • DEFA5 expression was inducible in Caco-2 cells.
  • miR-124 and miR-924 were found to bind to DEFA5.
  • Transfection with miR-124 and miR-924 mimics reduced DEFA5 mRNA and protein levels.

Conclusions:

  • miR-124 and miR-924 negatively regulate DEFA5 expression.
  • These miRNAs are implicated in the innate immune regulation of the intestine.
  • The findings suggest a role for miRNAs in the pathogenesis of IBD.