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Updated: Sep 13, 2025

Murine Colitis Modeling using Dextran Sulfate Sodium DSS

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Published on: January 19, 2010

PTEN Inactivation in Mouse Colonic Epithelial Cells Curtails DSS-Induced Colitis and Accelerates Recovery.

Larissa Kotelevets¹, Francine Walker², Godefroy Mamadou³

¹Sorbonne Université, Inserm, Centre de Recherche Saint-Antoine (CRSA), UMR_S938, 75012 Paris, France.

|July 29, 2025

Summary

Inactivating PTEN (phosphatase and tensin homolog) in intestinal epithelial cells alleviates experimental colitis in mice. This PTEN down-modulation enhances barrier function and promotes faster recovery from intestinal inflammation.

Keywords:

PTEN colitis dextran sulfate sodium (DSS)inflammation intestinal barrier junctional complexes mouse model tight junction tumor suppressor wound-healing

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Area of Science:

Gastroenterology
Molecular Biology
Immunology

Background:

PTEN is a crucial tumor suppressor regulating cell proliferation, differentiation, apoptosis, and invasiveness.
While PTEN down-modulation is linked to cancer, its transient inhibition may aid healing.
Investigating PTEN's role in intestinal epithelium is key to understanding inflammatory conditions.

Purpose of the Study:

To investigate the impact of PTEN invalidation in mouse intestinal epithelium.
To assess PTEN's role in experimental colitis induced by dextran sulfate sodium (DSS).
To explore PTEN's potential therapeutic role in intestinal inflammation.

Main Methods:

Conditional knockout of PTEN in intestinal epithelial cells of villin-Cre PTEN^flox/flox mice.
Induction of experimental colitis using dextran sulfate sodium (DSS).
Evaluation of inflammation markers, mucosal lesions, barrier function, and epithelial proliferation.

Main Results:

PTEN invalidation significantly alleviated DSS-induced experimental colitis.
Reduced weight loss, lower expression of inflammatory cytokines (IFN-γ, CXCL1, CXCL2), and diminished mucosal lesions were observed.
PTEN knockout enhanced intestinal barrier function by decreasing paracellular permeability and reinforcing claudin-3 expression, promoting faster recovery.

Conclusions:

PTEN inactivation demonstrates a protective effect against colitis onset.
Transient and localized PTEN down-modulation may be a viable strategy for promoting recovery from acute intestinal inflammation.