NDLI: Increased expression of the urokinase plasminogen activator system by Helicobacter pylori in gastric epithelial cells.

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Increased expression of the urokinase plasminogen activator system by Helicobacter pylori in gastric epithelial cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Kenny, Susan Duval, Cedric Sammut, Stephen J. Steele, Islay Pritchard, D. Mark Atherton, John C. Argent, Richard H. Dimaline, Rod Dockray, Graham J. Varro, Andrea
Description	Country affiliation: United kingdom Author Affiliation: Kenny S ( Physiological Laboratory, School of Biomedical Sciences, University of Liverpool, Crown St., Liverpool L69 3BX, UK.)
Abstract	The gastric pathogen Helicobacter pylori (H. pylori) is linked to peptic ulcer and gastric cancer, but the relevant pathophysiological mechanisms are unclear. We now report that H. pylori stimulates the expression of plasminogen activator inhibitor (PAI)-1, urokinase plasminogen activator (uPA), and its receptor (uPAR) in gastric epithelial cells and the consequences for epithelial cell proliferation. Real-time PCR of biopsies from gastric corpus, but not antrum, showed significantly increased PAI-1, uPA, and uPAR in H. pylori-positive patients. Transfection of primary human gastric epithelial cells with uPA, PAI-1, or uPAR promoters in luciferase reporter constructs revealed expression of all three in H+/K+ATPase- and vesicular monoamine transporter 2-expressing cells; uPA was also expressed in pepsinogen- and uPAR-containing trefoil peptide-1-expressing cells. In each case expression was increased in response to H. pylori and for uPA, but not PAI-1 or uPAR, required the virulence factor CagE. H. pylori also stimulated soluble and cell surface-bound uPA activity, and both were further increased by PAI-1 knockdown, consistent with PAI-1 inhibition of endogenous uPA. H. pylori stimulated epithelial cell proliferation, which was inhibited by uPA immunoneutralization and uPAR knockdown; exogenous uPA also stimulated proliferation that was further increased after PAI-1 knockdown. The proliferative effects of uPA were inhibited by immunoneutralization of the EGF receptor and of heparin-binding EGF (HB-EGF) by the mutant diphtheria toxin CRM197 and an EGF receptor tyrosine kinase inhibitor. H. pylori induction of uPA therefore leads to epithelial proliferation through activation of HB-EGF and is normally inhibited by concomitant induction of PAI-1; treatments directed at inhibition of uPA may slow the progression to gastric cancer.
File Format	HTM / HTML
ISSN	01931857
e-ISSN	15221547
DOI	10.1152/ajpgi.90283.2008
Journal	AJP: Gastrointestinal and Liver Physiology
Issue Number	3
Volume Number	295
Language	English
Publisher	American Physiological Society
Publisher Date	2008-09-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Physiology Discipline Gastroenterology Cell Proliferation Gastric Mucosa Microbiology Helicobacter Infections Helicobacter Pylori Isolation & Purification Plasminogen Activator Inhibitor 1 Metabolism Receptors, Cell Surface Urokinase-type Plasminogen Activator Bacterial Proteins Cell Transformation, Neoplastic Cells, Cultured Enzymology Pathology Genes, Reporter Pathogenicity Heparin-binding Egf-like Growth Factor Intercellular Signaling Peptides And Proteins Metalloproteases Genetics Precancerous Conditions Promoter Regions, Genetic Rna Interference Rna, Messenger Rna, Small Interfering Receptors, Urokinase Plasminogen Activator Stomach Neoplasms Transfection Up-regulation Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Hepatology Physiology Physiology (medical) Gastroenterology

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