Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Renewal of Intestinal Stem Cells

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...

Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal

Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal

Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.

Role Of Notch Signalling In Intestinal Stem Cell Renewal

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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Multifrequency tabletop magnetic resonance elastography for ex-vivo characterization of murine intestinal tissue biomechanics.

Journal of the mechanical behavior of biomedical materials·2026

Same author

Aligning patient and planetary health: planetary health diet adherence and inflammatory bowel disease prognosis across Western and Eastern cohorts.

NPJ science of food·2026

Same author

[Updated S3 guideline on ulcerative colitis].

Zeitschrift fur Gastroenterologie·2026

Same author

Mesenteric Adipose Tissue as a Modulator of Intestinal Inflammation: Mechanistic Insights and Model Systems in Crohn's Disease.

European journal of immunology·2026

Same author

Coordinated Interferon-γ/Tumor Necrosis Factor axis Drives Selective Loss of Activated Enteric Glia in Inflammatory Bowel Diseases.

Cellular and molecular gastroenterology and hepatology·2026

Same author

IBDome: An Integrated Molecular, Histopathological, and Clinical Atlas of Inflammatory Bowel Diseases.

Gastroenterology·2026

Search research articles

Related Experiment Video

Updated: Nov 7, 2025

Co-Culture of Murine Small Intestine Epithelial Organoids with Innate Lymphoid Cells

Co-Culture of Murine Small Intestine Epithelial Organoids with Innate Lymphoid Cells

Published on: March 23, 2022

Reprogramming Intestinal Epithelial Cell Polarity by Interleukin-22.

Deborah Delbue¹, Lydia Lebenheim¹, Danielle Cardoso-Silva¹

¹Department for Gastroenterology, Rheumatology and Infectious Diseases, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Berlin, Germany.

Frontiers in Medicine

|April 29, 2021

Summary

Interleukin-22 (IL-22) exposure impairs intestinal epithelial barrier function by disrupting tight junctions and promoting epithelial-mesenchymal transition (EMT). IL-22 exacerbates ileitis barrier defects, with the ERK pathway mediating these effects.

Keywords:

IL-22 MAPK barrier function cell polarity intestinal epithelial cells stat3 tight junctions

More Related Videos

Using Human Induced Pluripotent Stem Cell-derived Intestinal Organoids to Study and Modify Epithelial Cell Protection Against Salmonella and Other Pathogens

Using Human Induced Pluripotent Stem Cell-derived Intestinal Organoids to Study and Modify Epithelial Cell Protection Against Salmonella and Other Pathogens

Published on: May 12, 2019

Visualization of IL-22-expressing Lymphocytes Using Reporter Mice

Visualization of IL-22-expressing Lymphocytes Using Reporter Mice

Published on: January 25, 2017

Related Experiment Videos

Last Updated: Nov 7, 2025

Co-Culture of Murine Small Intestine Epithelial Organoids with Innate Lymphoid Cells

Co-Culture of Murine Small Intestine Epithelial Organoids with Innate Lymphoid Cells

Published on: March 23, 2022

Using Human Induced Pluripotent Stem Cell-derived Intestinal Organoids to Study and Modify Epithelial Cell Protection Against Salmonella and Other Pathogens

Using Human Induced Pluripotent Stem Cell-derived Intestinal Organoids to Study and Modify Epithelial Cell Protection Against Salmonella and Other Pathogens

Published on: May 12, 2019

Visualization of IL-22-expressing Lymphocytes Using Reporter Mice

Visualization of IL-22-expressing Lymphocytes Using Reporter Mice

Published on: January 25, 2017

Area of Science:

Gastroenterology
Immunology
Cell Biology

Background:

Interleukin-22 (IL-22) plays a role in intestinal epithelial integrity and is implicated in inflammatory bowel diseases (IBD) and colitis-associated cancer.
While IL-22 is known to protect the mucosal barrier and aid wound healing, its precise mechanisms in modulating intestinal epithelial cell polarity and tight junction assembly remain unclear.

Purpose of the Study:

To investigate the mechanisms by which IL-22 reprograms intestinal epithelia.
To determine if IL-22 modulates cell polarity and tight junction assembly in intestinal epithelial cells (IECs).

Main Methods:

IECs were treated with IL-22 in 2D cultures and 3D Matrigel® cyst models.
Barrier function, tight junction (TJ) assembly, cell polarity, migration, invasion, and epithelial-mesenchymal transition (EMT) were assessed.
In vivo studies utilized a Toxoplasma gondii-induced ileitis model in IL-22 knockout and wild-type mice.

Main Results:

IL-22 exposure induced barrier defects, impaired TJ protein expression and distribution, and delayed TJ reassembly.
In 3D models, IL-22 caused aberrant cyst formation and altered polarity protein localization.
IL-22 promoted cell migration, invasion, and EMT; the ERK pathway was identified as crucial for TJ barrier defects, while STAT3 was linked to cell survival.

Conclusions:

IL-22 impairs intestinal epithelial barrier integrity by inducing EMT, disrupting cell polarity, and increasing cell motility and invasion.
IL-22 mediates tight junctional barrier defects via the ERK signaling pathway.