Helicobacter pylori-Induced Loss of the Inhibitor-of-Apoptosis Protein Survivin Is Linked to Gastritis and Death of Human Gastric Cells

dc.contributor.authorValenzuela, Manuel
dc.contributor.authorPerez Perez, Guillermo
dc.contributor.authorCorvalan, Alejandro H.
dc.contributor.authorCarrasco, Gonzalo
dc.contributor.authorUrra, Hery
dc.contributor.authorBravo, Denisse
dc.contributor.authorToledo, Hector
dc.contributor.authorQuest, Andrew F. G.
dc.date.accessioned2024-01-10T12:05:46Z
dc.date.available2024-01-10T12:05:46Z
dc.date.issued2010
dc.description.abstractHelicobacter pylori infects the human stomach and modifies signaling pathways that affect gastric epithelial cell proliferation and viability. Chronic exposure to this pathogen contributes to the onset of gastric atrophy, an early event in the genesis of gastric cancer associated with H. pylori infection. Susceptibility to H. pylori-induced cell death ultimately depends on the presence of protective host cell factors. Although expression of the inhibitor-of-apoptosis protein survivin in adults is frequently linked to the development of cancer, evidence indicating that the protein is present in normal gastric mucosa is also available. Thus, we investigated in human gastric tissue samples and cell lines whether H. pylori infection is linked to loss of survivin and increased cell death. Our results show that infection with H. pylori decreased survivin protein levels in the mucosa of patients with gastritis. Furthermore, survivin down-regulation correlated with apoptosis and loss of cell viability in gastrointestinal cells cocultured with different H. pylori strains. Finally, overexpression of survivin in human gastric cells was sufficient to reduce cell death after infection. Taken together, these findings implicate survivin as an important survival factor in the gastric mucosa of humans.
dc.description.funderFondo de Investigacion Avanzada en Areas Prioritarias
dc.description.funderFondo Nacional de Investigacion Cientifica y Tecnologica
dc.fechaingreso.objetodigital2024-04-26
dc.format.extent10 páginas
dc.fuente.origenWOS
dc.identifier.doi10.1086/656143
dc.identifier.eissn1537-6613
dc.identifier.issn0022-1899
dc.identifier.pubmedidMEDLINE:20735270
dc.identifier.urihttps://doi.org/10.1086/656143
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/76066
dc.identifier.wosidWOS:000281912100006
dc.information.autorucMedicina;Carrasco G;S/I;14818
dc.information.autorucMedicina;Corvalan AH;S/I;63885
dc.issue.numero7
dc.language.isoen
dc.nota.accesocontenido parcial
dc.pagina.final1030
dc.pagina.inicio1021
dc.publisherOXFORD UNIV PRESS INC
dc.revistaJOURNAL OF INFECTIOUS DISEASES
dc.rightsacceso restringido
dc.subjectCAG PATHOGENICITY ISLAND
dc.subjectNITRIC-OXIDE SYNTHASE
dc.subjectVACUOLATING CYTOTOXIN
dc.subjectEXPRESSION
dc.subjectCANCER
dc.subjectCARCINOGENESIS
dc.subjectINFECTION
dc.subjectGENE
dc.subjectPATHWAY
dc.subjectGROWTH
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleHelicobacter pylori-Induced Loss of the Inhibitor-of-Apoptosis Protein Survivin Is Linked to Gastritis and Death of Human Gastric Cells
dc.typeartículo
dc.volumen202
sipa.codpersvinculados14818
sipa.codpersvinculados63885
sipa.indexWOS
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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