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Updated: May 31, 2026

Investigating Intestinal Barrier Breakdown in Living Organoids

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Published on: March 26, 2020

ABCG2 Upregulation Involving AKT/NF-κB Signaling Contributes to Intestinal Barrier Dysfunction in Inflammatory Bowel

Ping Shi^1,2, Juan Deng³, Xiaomei Song⁴

¹Chongqing Key Laboratory of Target-Based Drug Discovery and Research, Chongqing University of Technology, Chongqing, 400054, People's Republic of China.

Digestive Diseases and Sciences

|May 29, 2026

Summary

ABCG2 transporter upregulation exacerbates intestinal barrier dysfunction in inflammatory bowel disease (IBD). Inhibiting ABCG2 improves barrier integrity, highlighting it as a therapeutic target for IBD.

Keywords:

ATP-binding cassette subfamily G member 2 (ABCG2)Experimental colitis Inflammatory bowel disease (IBD)Intestinal barrier Tight junction proteins

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Published on: April 21, 2015

Area of Science:

Gastroenterology
Molecular Biology
Immunology

Background:

ATP-binding cassette subfamily G member 2 (ABCG2) is upregulated in inflammatory bowel disease (IBD) models.
Mechanisms regulating ABCG2 in inflammation and its role in intestinal barrier integrity are unclear.

Purpose of the Study:

Elucidate the signaling pathway for ABCG2 upregulation during inflammation.
Investigate ABCG2's functional role in intestinal barrier integrity in vitro and in vivo.

Main Methods:

Assessed intestinal epithelial barrier integrity using TEER and FITC-dextran permeability.
Analyzed tight junction proteins via immunofluorescence and immunoblotting.
Utilized Abcg2 knockout mice to study ABCG2's role in homeostasis.

Main Results:

Lipopolysaccharide (LPS) induced ABCG2 via AKT and NF-κB pathways.
Inhibiting or deleting ABCG2 enhanced barrier integrity (increased TEER, reduced permeability).
Abcg2 knockout improved colon length and reduced inflammation in IBD models.

Conclusions:

ABCG2 is a potential therapeutic target for inflammatory bowel disease (IBD).
Targeting ABCG2 may benefit patients with dysregulated transporter activity or genetic variants affecting drug response.