Ectodomain shedding of E-cadherin and c-Met is induced by Helicobacter pylori infection
Wiebke Schirrmeister1, Thorsten Gnad, Thomas Wex
1Clinic of Gastroenterology, Hepatology and Infectious Diseases, Otto-von-Guericke-University Magdeburg, Leipziger Str. 44, D-39120 Magdeburg, Germany.
Abstract:
Helicobacter pylori, a microaerophilic gram-negative bacterium, colonizes the human stomach. About 50% of the world's population is infected, and this infection is considered as the major risk factor for the development of gastric adenocarcinomas in 1% of infected subjects. Carcinogenesis is characterized by the process of epithelial-to-mesenchymal transition (EMT), in the course of which fully differentiated epithelial cells turn into depolarized and migratory cells. Concomitant disruption of adherence junctions (AJ) is facilitated by growth factors like hepatocyte growth factor 1 (HGF-1), but has been also shown to depend on ectodomain shedding of E-cadherin. The aim of this study was to investigate the impact of infection with H. pylori of NCI-N87 gastric epithelial cells on the shedding of E-cadherin and HGF-receptor c-Met. Our results show that infection with H. pylori provokes shedding of the surface proteins c-Met and E-cadherin. Evidence is provided that ADAM10 contributes to the shedding of c-Met and E-cadherin.
Related Concept Videos
Structure of Cadherins
Cadherins in Tissue Organization
Cell Sorting During Development
Cell sorting plays an...
Gastritis II: Pathophysiology
Adherens Junctions
Adherens Junctions are Dynamic
The endothelial cells...
Peptic Ulcer
Peptic Ulcer Disease II: Pathophysiology


