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Augmented intracellular glutathione inhibits fas-triggered apoptosis of activated human neutrophils

dc.rights.licenceAtribución-NoComercial 4.0 Internacional*
dc.contributor.authorWatson, R. William G.
dc.contributor.authorRotstein, Ori D.
dc.contributor.authorJiménez, María
dc.contributor.authorParodo, Jean
dc.contributor.authorMarshall, John C.
dc.date.accessioned2020-11-09T02:55:40Z
dc.date.available2020-11-09T02:55:40Z
dc.date.created1997-06-01
dc.identifierhttps://ashpublications.org/blood/article/89/11/4175/138904/Augmented-Intracellular-Glutathione-Inhibits-Fasspa
dc.identifier.issn0006-4971 / 1528-0020 (Electrónico)spa
dc.identifier.urihttp://hdl.handle.net/10554/51638
dc.formatPDFspa
dc.format.mimetypeapplication/pdfspa
dc.language.isoengspa
dc.rights.urihttp://creativecommons.org/licenses/by-nc/4.0/*
dc.titleAugmented intracellular glutathione inhibits fas-triggered apoptosis of activated human neutrophilsspa
dc.type.hasversionhttp://purl.org/coar/version/c_ab4af688f83e57aa
dc.description.quartilewosQ1spa
dc.description.quartilescopusQ1spa
dc.identifier.doihttps://doi.org/10.1182/blood.V89.11.4175spa
dc.subject.keywordApoptosisspa
dc.subject.keywordGlutathionespa
dc.subject.keywordNeutrophilsspa
dc.subject.keywordIntegrinsspa
dc.subject.keywordCross-linkingspa
dc.subject.keywordDeathspa
dc.subject.keywordNeutrophil apoptosisspa
dc.description.abstractenglishAgonist signals delivered through cell surface Fas induce apoptosis. However, the apoptotic program can be modulated by signals from the environment, and in particular, by signals delivered through adhesion molecules. Because neutrophil functional activity in inflammation is contingent on cell survival, and because circulating neutrophils normally die rapidly through a constitutively expressed apoptotic program, we evaluated Fas-mediated apoptosis in resting and inflammatory human neutrophils. We show that normal neutrophils respond to Fas engagement with accelerated rates of apoptosis, but cross-linking of β2 integrins or priming with bacterial lipopolysaccharide (LPS) prevents this increase. Adhesion molecule cross-linking results in increased intracellular glutathione (GSH). Augmentation of intracellular GSH with exogenous GSH or N-acetylcysteine is sufficient to reduce the Fas-triggered increase in apoptotic rates. Prevention of the activation induced GSH increase by buthionine sulfoximine, a cell permeable inhibitor of GSH biosynthesis, restored Fas responsiveness in activated neutrophils, an effect that could be blocked with exogenous GSH. Taken together, these data show that Fas-induced signaling for neutrophil apoptosis is blocked in a redox sensitive manner by costimulatory signals delivered through β2 integrins or activation by LPS, and provide a biologic explanation for sustained neutrophil survival in the inflammatory environment.spa
dc.type.localArtículo de revistaspa
dc.contributor.corporatenamePontificia Universidad Javeriana. Facultad de Medicina. Departamento de Cirugía y Especialidades. Grupo de Investigación de Cirugía y Especialidades
dc.identifier.instnameinstname:Pontificia Universidad Javerianaspa
dc.identifier.reponamereponame:Repositorio Institucional - Pontificia Universidad Javerianaspa
dc.identifier.repourlrepourl:https://repository.javeriana.edu.cospa
dc.type.coarhttp://purl.org/coar/resource_type/c_6501spa
dc.relation.citationstartpage4175spa
dc.relation.citationendpage4181spa
dc.relation.ispartofjournalBloodspa
dc.description.indexingRevista Nacional - Indexadaspa
dc.relation.citationvolume89spa
dc.relation.citationissue11spa
dc.rights.coarhttp://purl.org/coar/access_right/c_abf2spa


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