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dc.contributor.authorAbdel-Latif, M.M.M.
dc.contributor.authorWindle, H. J.
dc.contributor.authorFitzgerald, Katherine A.
dc.contributor.authorAng, Y. S.
dc.contributor.authorEidhin, D. Ni
dc.contributor.authorLi-Weber, M.
dc.contributor.authorSabra, K.
dc.contributor.authorKelleher, Daniel J.
dc.date2022-08-11T08:09:11.000
dc.date.accessioned2022-08-23T16:20:21Z
dc.date.available2022-08-23T16:20:21Z
dc.date.issued2004-05-25
dc.date.submitted2011-03-25
dc.identifier.citationInfect Immun. 2004 Jun;72(6):3549-60. <a href="http://dx.doi.org/10.1128/IAI.72.6.3549-3560.2004">Link to article on publisher's site</a>
dc.identifier.issn0019-9567 (Linking)
dc.identifier.doi10.1128/IAI.72.6.3549-3560.2004
dc.identifier.pmid15155664
dc.identifier.urihttp://hdl.handle.net/20.500.14038/35263
dc.description.abstractThe early growth response 1 (Egr-1) transcription factor is rapidly induced by various stimuli and is implicated in the regulation of cell growth, differentiation, and gene expression. The aim of this study was to examine the effect of Helicobacter pylori on the expression of Egr-1 and Egr-1-regulated genes in gastric epithelial AGS cells. Egr-1 expression was assayed by immunoblotting and electrophoretic mobility shift assays using H. pylori-stimulated AGS cells. Transient transfection experiments with promoter-reporter constructs of CD44, ICAM-1, and CD95L were used for expression studies. H. pylori induced the expression of Egr-1 in gastric epithelial cell lines in a dose-dependent manner, with the rapid kinetics that are typical of this class of transcription factors. Immunohistochemical studies of biopsies revealed that Egr-1 expression is more abundant in H. pylori-positive patients than in uninfected individuals. Reporter-promoter transfection studies indicated that Egr-1 binding is required for the H. pylori-induced transcriptional promoter activity of the CD44, ICAM-1, and CD95L (APO-1/Fas) constructs. The blocking of egr-1 with an antisense sequence prevented H. pylori-induced Egr-1 and CD44 protein expression. The MEK1/2 signaling cascade participates in H. pylori-mediated Egr-1 expression, but the p38 pathway does not. The data indicate that H. pylori induces Egr-1 expression in AGS cells in vitro and that the Egr-1 protein is readily detectable in biopsies from H. pylori-positive subjects. These observations suggest that H. pylori-associated Egr-1 expression may play a role, in part, in H. pylori-induced pathology.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=15155664&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1128/IAI.72.6.3549-3560.2004
dc.subjectAntigens, CD44
dc.subjectCell Line, Tumor
dc.subjectCoculture Techniques
dc.subjectDNA-Binding Proteins
dc.subjectEarly Growth Response Protein 1
dc.subjectEpithelial Cells
dc.subjectFas Ligand Protein
dc.subjectGastric Mucosa
dc.subject*Gene Expression Regulation
dc.subjectGenes, Reporter
dc.subjectHelicobacter Infections
dc.subjectHelicobacter pylori
dc.subjectHumans
dc.subjectImmediate-Early Proteins
dc.subjectImmunohistochemistry
dc.subjectIntercellular Adhesion Molecule-1
dc.subjectMembrane Glycoproteins
dc.subjectPromoter Regions, Genetic
dc.subjectTranscription Factors
dc.subjectTransfection
dc.subjectImmunology and Infectious Disease
dc.titleHelicobacter pylori activates the early growth response 1 protein in gastric epithelial cells
dc.typeJournal Article
dc.source.journaltitleInfection and immunity
dc.source.volume72
dc.source.issue6
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/infdis_pp/96
dc.identifier.contextkey1901420
html.description.abstract<p>The early growth response 1 (Egr-1) transcription factor is rapidly induced by various stimuli and is implicated in the regulation of cell growth, differentiation, and gene expression. The aim of this study was to examine the effect of Helicobacter pylori on the expression of Egr-1 and Egr-1-regulated genes in gastric epithelial AGS cells. Egr-1 expression was assayed by immunoblotting and electrophoretic mobility shift assays using H. pylori-stimulated AGS cells. Transient transfection experiments with promoter-reporter constructs of CD44, ICAM-1, and CD95L were used for expression studies. H. pylori induced the expression of Egr-1 in gastric epithelial cell lines in a dose-dependent manner, with the rapid kinetics that are typical of this class of transcription factors. Immunohistochemical studies of biopsies revealed that Egr-1 expression is more abundant in H. pylori-positive patients than in uninfected individuals. Reporter-promoter transfection studies indicated that Egr-1 binding is required for the H. pylori-induced transcriptional promoter activity of the CD44, ICAM-1, and CD95L (APO-1/Fas) constructs. The blocking of egr-1 with an antisense sequence prevented H. pylori-induced Egr-1 and CD44 protein expression. The MEK1/2 signaling cascade participates in H. pylori-mediated Egr-1 expression, but the p38 pathway does not. The data indicate that H. pylori induces Egr-1 expression in AGS cells in vitro and that the Egr-1 protein is readily detectable in biopsies from H. pylori-positive subjects. These observations suggest that H. pylori-associated Egr-1 expression may play a role, in part, in H. pylori-induced pathology.</p>
dc.identifier.submissionpathinfdis_pp/96
dc.contributor.departmentDepartment of Biochemistry and Molecular Pharmacology
dc.contributor.departmentDepartment of Medicine, Division of Infectious Diseases and Immunology
dc.source.pages3549-60


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