| Autor: |
Lapointe, Tamia K., O'Connor, Pamela M., Feener, Troy D., Menard, Daniel, Buret, Andre G. |
| Předmět: |
|
| Zdroj: |
FASEB Journal; Apr2007, Vol. 21 Issue 5, pA191-A191, 1/5p |
| Abstrakt: |
The ability of H. pylori (Hp) to disrupt the gastric epithelial barrier may contribute to the development of gastroduodenal ulcers and gastric adenocarcinomas. The direct effects of Hp on the gastric epithelium remain incompletely understood. Internalization of TJ proteins promotes the rapid loss of intercellular adhesion and a subsequent increase in epithelial permeability. Aim: The aim of this study was to investigate the mechanisms involved in Hp-induced disruption of epithelial barrier structure and function in vitro using the human gastric epithelial (HGE-20) cell line. Results: Hp strain SS1 significantly increased transepithelial fluxes of FITC-dextran. Immunocytochemistry and western blotting demonstrated golgi apparatus-associated accumulation of claudin-4 in the cytoplasm, which coincided with the loss of claudin-4 from the cell membrane. Pharmacological inhibition of de novo protein synthesis as well as the blocking of clathrin-coated pit endocytosis prevented these effects. Infection with Hp also increased Rho kinase expression and activity, and inhibition of Rho kinase reduced loss of claudin-4 from the membrane. Conclusion: The mechanisms by which lip disrupts the gastric epithelial barrier involve membrane-to-cytosol translocation of claudin-4. This effect is mediated by clathrin-coated pit endocytosis and depends, at least in part, on Rho kinase. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
|
Plný text