Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2004-3-3
pubmed:abstractText
The gastric pathogen Helicobacter pylori is associated with a progression to gastric cancer. The specific targets of H. pylori that might influence this progression are still unclear. Previous studies indicated that the gastric hormone gastrin, which may be increased in H. pylori infection, stimulates gastric expression of plasminogen activator inhibitor (PAI)-2, which is an inhibitor of the urokinase plasminogen activator and has previously been shown to be increased in gastric adenocarcinoma. Here, we report that H. pylori also increases PAI-2 expression. In gastric biopsies of H. pylori-positive subjects there was increased PAI-2, including subjects with plasma gastrin concentrations in the normal range. PAI-2 was expressed mainly in chief and mucous cells. In a gastric cancer cell line (AGS), H. pylori increased PAI-2 expression, which was associated with inhibition of H. pylori-stimulated cell invasion and apoptosis. The induction of PAI-2 by H. pylori was mediated by release of interleukin-8 and activation of cyclooxygenase-2, and interestingly, gastrin stimulated PAI-2 expression by similar paracrine pathways. The activation of NFkappaB was required for interleukin-8 and cyclooxygenase-2 activation but did not occur in cells responding to these paracrine mediators. The data suggest that induction of PAI-2 is a specific target in H. pylori infection, mediated at least partly by paracrine factors; induction of PAI-2 inhibits cell invasion and apoptosis and is a candidate for influencing the progression to gastric cancer.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
64
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1695-702
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:14996729-Aged, pubmed-meshheading:14996729-Apoptosis, pubmed-meshheading:14996729-Cyclooxygenase 2, pubmed-meshheading:14996729-Female, pubmed-meshheading:14996729-Gastric Mucosa, pubmed-meshheading:14996729-Helicobacter pylori, pubmed-meshheading:14996729-Humans, pubmed-meshheading:14996729-Interleukin-8, pubmed-meshheading:14996729-Isoenzymes, pubmed-meshheading:14996729-Male, pubmed-meshheading:14996729-Membrane Proteins, pubmed-meshheading:14996729-Middle Aged, pubmed-meshheading:14996729-NF-kappa B, pubmed-meshheading:14996729-Neoplasm Invasiveness, pubmed-meshheading:14996729-Plasminogen Activator Inhibitor 2, pubmed-meshheading:14996729-Prostaglandin-Endoperoxide Synthases, pubmed-meshheading:14996729-Protein Transport, pubmed-meshheading:14996729-Stomach Neoplasms
pubmed:year
2004
pubmed:articleTitle
Helicobacter pylori induces plasminogen activator inhibitor 2 in gastric epithelial cells through nuclear factor-kappaB and RhoA: implications for invasion and apoptosis.
pubmed:affiliation
Physiological Laboratory, University of Liverpool, Liverpool, United Kingdom.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't