Related Experiment Video

Updated: Sep 2, 2025

Functional Assessment of Intestinal Permeability and Neutrophil Transepithelial Migration in Mice using a Standardized Intestinal Loop Model
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Functional Assessment of Intestinal Permeability and Neutrophil Transepithelial Migration in Mice using a Standardized Intestinal Loop Model

Published on: February 11, 2021

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Epithelial JAM-A is fundamental for intestinal wound repair in vivo

Shuling Fan, Kevin Boerner, Chithra K Muraleedharan

    JCI Insight
    |August 9, 2022
    PubMed

    Insights

    Junctional adhesion molecule-A (JAM-A) is crucial for intestinal healing. Loss of JAM-A impairs mucosal repair by disrupting cell migration and focal adhesion dynamics in epithelial cells.

    Area of Science:

    • Gastroenterology
    • Cell Biology
    • Immunology

    Background:

    • Junctional adhesion molecule-A (JAM-A) is expressed in intestinal epithelial cells (IECs) and regulates barrier function.
    • Previous in vitro studies suggest JAM-A promotes IEC migration, but its in vivo role in healing remains unclear.

    Purpose of the Study:

    • To investigate the in vivo role of JAM-A in intestinal mucosal wound repair using a novel mouse model.
    • To elucidate the molecular mechanisms by which JAM-A influences epithelial cell migration during healing.

    Main Methods:

    • Developed an inducible intestinal epithelial-specific JAM-A-knockdown mouse model (Jam-aERΔIEC).
    • Assessed mucosal healing after chemically induced colitis and colonic biopsy wounding.
    • Performed in vitro wound healing assays with JAM-A-deficient primary IECs.
    • Analyzed focal adhesion complex composition and activity (Rap1A, Talin, β1 integrin).

    Main Results:

    • IEC-specific JAM-A loss did not cause spontaneous colitis but significantly impaired mucosal healing in vivo.
    • JAM-A-deficient IECs exhibited reduced migration in vitro.
    • Loss of JAM-A disrupted the stabilization of Rap1A/Talin/β1 integrin signaling complexes at focal adhesions.
    • Reduced Rap1A activity, Talin, and β1 integrin levels were observed in JAM-A-deficient IECs, along with fewer focal adhesions.

    Conclusions:

    • Epithelial JAM-A is essential for effective in vivo intestinal mucosal repair.
    • JAM-A regulates mucosal healing by controlling focal adhesion dynamics and epithelial cell migration.
    • Targeting JAM-A may offer therapeutic potential for enhancing intestinal wound healing.

    Keywords:
    Cell BiologyGastroenterologyInflammatory bowel disease

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