Journal
FASEB JOURNAL
Volume 21, Issue 1, Pages 197-206Publisher
FEDERATION AMER SOC EXP BIOL
DOI: 10.1096/fj.06-6801com
Keywords
epithelial permeability; inflammatory bowel diseases; glutathione
Categories
Funding
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R24DK064399] Funding Source: NIH RePORTER
- NIDDK NIH HHS [R24-DK-064399] Funding Source: Medline
- PHS HHS [R01-DKO 6411] Funding Source: Medline
Ask authors/readers for more resources
Prohibitin (PHB) is an evolutionarily conserved and ubiquitously expressed protein whose expression or function in intestinal diseases is not known. In this study, we examined the expression and role of PHB in oxidative stress associated with inflammatory bowel disease. Our results show that PHB primarily localizes to the mitochondria in intestinal epithelial cells. Its expression is down-regulated during active human Crohn's disease, experimental colitis in vivo, and oxidative stress in vitro. PHB overexpression increases the expression of glutathione-S-transferase pi and protects from oxidant-induced depletion of glutathione. Finally, PHB overexpression decreases accumulation of reactive oxygen metabolites, as well as increased permeability induced by oxidative stress in intestinal epithelial cells. Together, these results suggest that PHB constitutes a previously unrecognized cellular defense against oxidant injury. Thus, strategies to modulate PHB levels may constitute a novel therapeutic approach for intestinal inflammatory diseases, wherein oxidative stress plays a critical role in tissue injury and inflammation.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available