ArticleGastroenterology2007
Pattern of transcription factor activation in Helicobacter pylori-infected Mongolian gerbils.
Article in Gastroenterology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 38 citations in OpenAlex.
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- Helicobacter pylori infection, gastrin and cyclooxygenase-2 in gastric carcinogenesis.World journal of gastroenterology · 2014Review
- Potential mechanism of corpus-predominant gastritis after PPI therapy in Helicobacter pylori-positive patients with GERD.World journal of gastroenterology · 2014Review
- Helicobacter pylori virulence and cancer pathogenesis.Future oncology (London, England) · 2014Review
- Identification of the genes that contribute to lactate utilization in Helicobacter pylori.PloS one · 2014Article
- The significance of virulence factors in Helicobacter pylori.Journal of digestive diseases · 2013Review
- Helicobacter bilis gamma-glutamyltranspeptidase enhances inflammatory stress response via oxidative stress in colon epithelial cells.PloS one · 2013Article
- Arginine and polyamines in Helicobacter pylori-induced immune dysregulation and gastric carcinogenesis.Amino acids · 2012Article
- Pathogenesis of Helicobacter pylori-Related Gastroduodenal Diseases from Molecular Epidemiological Studies.Gastroenterology research and practice · 2012Article
- Helicobacter pylori outer membrane proteins on gastric mucosal interleukin 6 and 11 expression in Mongolian gerbils.Journal of gastroenterology and hepatology · 2011Article
- Effects of blood group antigen-binding adhesin expression during Helicobacter pylori infection of Mongolian gerbils.The Journal of infectious diseases · 2011Article
- Mechanisms of disease: Helicobacter pylori virulence factors.Nature reviews. Gastroenterology & hepatology · 2010Review
- Helicobacter pylori induction of the gastrin promoter through GC-rich DNA elements.Helicobacter · 2010Article
- Helicobacter pylori induces ERK-dependent formation of a phospho-c-Fos c-Jun activator protein-1 complex that causes apoptosis in macrophages.The Journal of biological chemistry · 2010Article
- Clinical relevance of cagPAI intactness in Helicobacter pylori isolates from Vietnam.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2010Article
- Regulation of the Helicobacter pylori cellular receptor decay-accelerating factor.The Journal of biological chemistry · 2008Article
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
BACKGROUND AND
aimsHelicobacter pylori interact with epithelial cells resulting in activation of cellular signaling pathways leading to an inflammatory response. The pattern and timing of transcription factor activation in H pylori-infected gastric mucosa remain unclear. We investigated the roles of transcription factors in the gastric mucosa of H pylori-infected gerbils over the course of the infection.
methodsSix-week-old male Mongolian gerbils were inoculated orally with H pylori TN2GF4 or isogenic cagE mutants and examined at 1, 3, 9, and 18 months. We examined the expression of 54 transcription factors using DNA/protein arrays and electrophoretic mobility shift assays. Phosphorylation status of mitogen-activated protein kinases and IkappaB were evaluated by immunoblot and immunohistochemistry.
resultsTen transcription factors were up-regulated by H pylori infection. Six of these factors, including activator protein-1 (AP-1) and cAMP responsive element binding protein (CREB), reached maximal levels at 3 months and were strongly correlated with cellular inflammation and ulceration. Phosphorylation of extracellular signal-regulated kinase correlated with activation of AP-1 and CREB. Levels of nuclear factor-kappaB and interferon-stimulated responsive element (ISRE) peaked at 18 months and correlated with the presence of severe atrophy and with phosphorylation of Jun-N-terminal kinase (JNK), p38, and IkappaB.
conclusionsThe gastric mucosal transcription factors induced by H pylori infection differed according to the phase and outcome of infection; AP-1 and CREB levels were early responders related to inflammation and ulceration, whereas NF-kappaB and ISRE were late responders related to atrophy.
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