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Wip1 protects hydrogen peroxide-induced colonic epithelial barrier dysfunction.
- Source :
- Cellular & Molecular Life Sciences; Dec2007, Vol. 64 Issue 23, p3139-3147, 9p, 1 Color Photograph, 5 Graphs
- Publication Year :
- 2007
-
Abstract
- Tight junctions (TJs) create a paracellular permeability barrier. Although reactive oxygen species have been implicated as mediators of inflammation in inflammatory bowel diseases, their influence on the function of colonic epithelial TJs remains unknown. Oxidative stress-mediated colonic epithelial permeability was significantly attenuated by a p38 mitogen-activated protein (MAP) kinase inhibitor, SB203580. Although the amount of TJ proteins was not altered, hydrogen peroxide (H<subscript>2</subscript>O<subscript>2</subscript>) changed the localization of claudin-4 protein from an NP-40 insoluble fraction to a soluble fraction and from an apical TJ to lateral membrane. The p38 MAP kinase inactivator Wip1 significantly attenuated phosphorylation of p38 MAP kinase, and oxidative stress mediated permeability. H<subscript>2</subscript>O<subscript>2</subscript>-induced changes in claudin-4 localization were abolished by SB203580 pretreatment as well as Wip1-expressing adenovirus infection. This is the first study to demonstrate that exogenous Wip1 functions to protect oxidative stress-mediated colonic mucosal permeability and that H<subscript>2</subscript>O<subscript>2</subscript>-induced claudin-4 dislocalization is abolished by Wip1. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 1420682X
- Volume :
- 64
- Issue :
- 23
- Database :
- Complementary Index
- Journal :
- Cellular & Molecular Life Sciences
- Publication Type :
- Academic Journal
- Accession number :
- 28547542
- Full Text :
- https://doi.org/10.1007/s00018-007-7268-7