Prohibitin 1 modulates mitochondrial stress-related autophagy in human colonic epithelial cells.

PloS One
Arwa S KathiriaArianne L Theiss

Abstract

Autophagy is an adaptive response to extracellular and intracellular stress by which cytoplasmic components and organelles, including damaged mitochondria, are degraded to promote cell survival and restore cell homeostasis. Certain genes involved in autophagy confer susceptibility to Crohn's disease. Reactive oxygen species and pro-inflammatory cytokines such as tumor necrosis factor α (TNFα), both of which are increased during active inflammatory bowel disease, promote cellular injury and autophagy via mitochondrial damage. Prohibitin (PHB), which plays a role in maintaining normal mitochondrial respiratory function, is decreased during active inflammatory bowel disease. Restoration of colonic epithelial PHB expression protects mice from experimental colitis and combats oxidative stress. In this study, we investigated the potential role of PHB in modulating mitochondrial stress-related autophagy in intestinal epithelial cells. We measured autophagy activation in response to knockdown of PHB expression by RNA interference in Caco2-BBE and HCT116 WT and p53 null cells. The effect of exogenous PHB expression on TNFα- and IFNγ-induced autophagy was assessed. Autophagy was inhibited using Bafilomycin A(1) or siATG16L1 during PHB kn...Continue Reading

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Citations

Apr 2, 2014·Journal of Clinical Biochemistry and Nutrition·Hiromu ItoIchinosuke Hyodo
Mar 16, 2013·American Journal of Physiology. Gastrointestinal and Liver Physiology·Arwa S KathiriaArianne L Theiss
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Methods Mentioned

BETA
biopsies
transfection
flow cytometry
confocal microscopy
PCR
electrophoresis
fluorescence microscopy

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