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Related Experiment Video

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Investigating Intestinal Barrier Breakdown in Living Organoids
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Published on: March 26, 2020

AMP-activated protein kinase mediates the interferon-gamma-induced decrease in intestinal epithelial barrier

Michael Scharl1, Gisela Paul1, Kim E Barrett1

  • 1Department of Medicine, University of California, San Diego, School of Medicine, La Jolla, California 92093.

The Journal of Biological Chemistry
|August 6, 2009
PubMed
Summary
This summary is machine-generated.

AMP-activated protein kinase (AMPK) plays a role in inflammatory bowel disease by mediating the effects of interferon-gamma (IFNgamma) on intestinal epithelial barrier function.

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Published on: February 11, 2021

Area of Science:

  • Gastroenterology
  • Cell Biology
  • Molecular Medicine

Background:

  • Impaired intestinal epithelial barrier function is central to inflammatory bowel disease (IBD) pathogenesis.
  • Interferon-gamma (IFNgamma), a pro-inflammatory cytokine, is implicated in Crohn disease and disrupts epithelial barrier integrity.
  • The precise signaling pathways linking IFNgamma to barrier dysfunction remain incompletely understood.

Purpose of the Study:

  • To investigate the role of AMP-activated protein kinase (AMPK) in mediating the effects of IFNgamma on intestinal epithelial barrier function.
  • To determine if AMPK activation is necessary for IFNgamma-induced changes in barrier properties and tight junction protein expression.

Main Methods:

  • T(84) intestinal epithelial cells were treated with IFNgamma.
  • AMPK activation was assessed by phosphorylation.
  • AMPK was inhibited using pharmacological inhibitors or knockdown.
  • Epithelial barrier function was measured by transepithelial electrical resistance (TER) and permeability.
  • Expression of tight junction proteins (occludin, ZO-1) was analyzed.

Main Results:

  • IFNgamma treatment activated AMPK in T(84) cells via phosphorylation, independent of cellular energy status.
  • Inhibition or knockdown of AMPK partially or fully prevented IFNgamma-induced decreases in TER and increases in permeability.
  • AMPK activation was necessary for the IFNgamma-mediated downregulation of occludin and ZO-1 expression.
  • AMPK activation alone did not alter epithelial barrier function.

Conclusions:

  • AMPK acts in concert with other IFNgamma-induced signals to mediate the disruption of intestinal epithelial barrier function.
  • These findings highlight a novel role for AMPK in the pathogenesis of chronic intestinal inflammation, potentially implicating it in IBD.
  • Targeting AMPK may offer a therapeutic strategy for managing inflammatory bowel disease.