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dc.contributor.authorManzo, Barbara Ada
dc.contributor.authorCrabtree, Jean E
dc.contributor.authorFiona Campbell, M
dc.contributor.authorTweedle, David
dc.contributor.authorPotten, Christopher S
dc.contributor.authorBajaj-Elliott, Mona
dc.contributor.authorSanderson, Ian R
dc.contributor.authorWilson, James W
dc.date.accessioned2009-07-06T15:50:58Z
dc.date.available2009-07-06T15:50:58Z
dc.date.issued2006-04
dc.identifier.citationHelicobacter pylori regulates the expression of inhibitors of DNA binding (Id) proteins by gastric epithelial cells. 2006, 8 (4):1064-74 Microbes Infect.en
dc.identifier.issn1286-4579
dc.identifier.pmid16473539
dc.identifier.doi10.1016/j.micinf.2005.11.003
dc.identifier.urihttp://hdl.handle.net/10541/72626
dc.description.abstractId transcription factors control proliferation, differentiation and apoptosis by inhibiting the DNA binding of basic helix-loop-helix transcription factors. Increased expression of Id proteins promotes proliferation, inhibits differentiation, and is associated with intestinal tumorigenesis. We aimed to determine how Helicobacter pylori may alter the expression of Id proteins by gastric epithelial cells: it was hypothesised that H. pylori, a known carcinogen, would result in increased expression of one or more Id family members. In vitro and in vivo models of infection were employed, including treatment of AGS gastric epithelial cells with wild-type H. pylori strains, 60190 and SS1, and Mongolian gerbils infected with H. pylori SS1. A small cohort of human gastric mucosal biopsies was also examined. Treatment of AGS cells with H. pylori resulted in down-regulation of Id1 and Id3. Unexpectedly, expression of the main target of Id proteins, the basic helix-loop-helix transcription factor E2A, was also suppressed, with an associated decrease in E-box binding activity. In contrast, H. pylori induced the expression of the CDK inhibitor p21(WAF-1/cip1), and the homeobox transcription factor, Cdx2, an early marker of intestinal metaplasia of the stomach epithelium. Gastric epithelium from H. pylori-infected gerbils demonstrated similar changes, with decreased Id2, Id3 and E2A, and elevated p21(WAF-1/cip1) expression. In human gastric epithelium also, H. pylori infection was associated with reduced Id and E2A expression. In conclusion, H. pylori alters the expression of Id proteins, in vitro and in vivo; it is hypothesised that these changes contribute to H. pylori-associated pathologies.
dc.language.isoenen
dc.subjectCell Line Tumouren
dc.subject.meshAdolescent
dc.subject.meshAdult
dc.subject.meshAged
dc.subject.meshAnimals
dc.subject.meshBasic Helix-Loop-Helix Transcription Factors
dc.subject.meshBiopsy
dc.subject.meshBlotting, Western
dc.subject.meshCell Line, Tumor
dc.subject.meshCyclin-Dependent Kinase Inhibitor p21
dc.subject.meshDNA-Binding Proteins
dc.subject.meshDown-Regulation
dc.subject.meshDyspepsia
dc.subject.meshEpithelial Cells
dc.subject.meshFemale
dc.subject.meshGerbillinae
dc.subject.meshHelicobacter Infections
dc.subject.meshHelicobacter pylori
dc.subject.meshHomeodomain Proteins
dc.subject.meshHumans
dc.subject.meshImmunohistochemistry
dc.subject.meshInhibitor of Differentiation Proteins
dc.subject.meshMiddle Aged
dc.subject.meshRNA
dc.subject.meshReverse Transcriptase Polymerase Chain Reaction
dc.subject.meshStomach
dc.titleHelicobacter pylori regulates the expression of inhibitors of DNA binding (Id) proteins by gastric epithelial cells.en
dc.typeArticleen
dc.contributor.departmentResearch Centre for Gastroenterology, Institute of Cell and Molecular Sciences, Barts and The London, Queen Mary's School of Medicine and Dentistry, University of London, 4 Newark Street, London E1 2AT,UK.en
dc.identifier.journalMicrobes and Infectionen
html.description.abstractId transcription factors control proliferation, differentiation and apoptosis by inhibiting the DNA binding of basic helix-loop-helix transcription factors. Increased expression of Id proteins promotes proliferation, inhibits differentiation, and is associated with intestinal tumorigenesis. We aimed to determine how Helicobacter pylori may alter the expression of Id proteins by gastric epithelial cells: it was hypothesised that H. pylori, a known carcinogen, would result in increased expression of one or more Id family members. In vitro and in vivo models of infection were employed, including treatment of AGS gastric epithelial cells with wild-type H. pylori strains, 60190 and SS1, and Mongolian gerbils infected with H. pylori SS1. A small cohort of human gastric mucosal biopsies was also examined. Treatment of AGS cells with H. pylori resulted in down-regulation of Id1 and Id3. Unexpectedly, expression of the main target of Id proteins, the basic helix-loop-helix transcription factor E2A, was also suppressed, with an associated decrease in E-box binding activity. In contrast, H. pylori induced the expression of the CDK inhibitor p21(WAF-1/cip1), and the homeobox transcription factor, Cdx2, an early marker of intestinal metaplasia of the stomach epithelium. Gastric epithelium from H. pylori-infected gerbils demonstrated similar changes, with decreased Id2, Id3 and E2A, and elevated p21(WAF-1/cip1) expression. In human gastric epithelium also, H. pylori infection was associated with reduced Id and E2A expression. In conclusion, H. pylori alters the expression of Id proteins, in vitro and in vivo; it is hypothesised that these changes contribute to H. pylori-associated pathologies.


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