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Oxidative stress attenuates Fas-mediated apoptosis in Jurkat T cell line through Bfl-1 induction

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dc.contributor.authorKim, Heejung-
dc.contributor.authorKim, Yong-Nyun-
dc.contributor.authorKim, Hyungsoo-
dc.contributor.authorKim, Chul-Woo-
dc.date.accessioned2009-09-22T13:31:17Z-
dc.date.available2009-09-22T13:31:17Z-
dc.date.issued2004-12-14-
dc.identifier.citationOncogene 24: 1252-1261en
dc.identifier.issn0950-9232-
dc.identifier.urihttps://hdl.handle.net/10371/9686-
dc.description.abstractMany types of mammalian cells produce ROS in response to many different stimuli to modulate a number of cellular functions, including apoptosis. However, the correlation between ROS and apoptosis remains controversial, and the mechanisms whereby ROS-induced signals are propagated to critical downstream targets remain largely undefined. Here, we demonstrate that hydrogen peroxide (H2O2) upregulates the expression of Bfl-1, an antiapoptotic member of the Bcl-2 family, and that this is responsible for the antiapoptotic activity of ROS. When Jurkat, human leukemic T cells, were pretreated with 100 microM H2O2 and then treated with anti-Fas antibody, apoptosis was impaired without change of cell surface Fas expression. An investigation of the expression patterns of Bcl-2 family genes revealed that H2O2 treatment induced Bfl-1 gene expression, but left other genes unchanged, and this Bfl-1 expression and H2O2 -induced antiapoptotic effect was inhibited by antioxidants or NF-kappaB inhibitor. In addition, an electromobility shift assay revealed that the p65/p50 subunits of NF-kappaB activated by H2O2 bound to a bfl-1 promoter. Neither the induction of Bfl-1 nor the antiapoptotic effect of H2O2 was detected in Bfl-1-knockdown Jurkat cell line containing Bfl-1 antisense (Bfl-1AS). These data indicate that oxidative stress induces the expression of Bfl-1 via NF-kappaB activation, and this early-response gene protects cells from Fas-mediated apoptosis. This may be a cellular survival mechanism of cells exposed to phagocytes-derived ROS.en
dc.description.sponsorshipThis work was supported by the Korea Science & Engineering
Foundation (KOSEF) through the Tumor Immunity Medical
Research Center at Seoul National University College of
Medicine.
en
dc.language.isoen-
dc.publisherNature Publishing Groupen
dc.subjecthydrogen peroxideen
dc.subjectapoptosisen
dc.subjectBfl-1en
dc.subjectNF-kappaBen
dc.titleOxidative stress attenuates Fas-mediated apoptosis in Jurkat T cell line through Bfl-1 inductionen
dc.typeArticleen
dc.contributor.AlternativeAuthor김희정-
dc.contributor.AlternativeAuthor김용년-
dc.contributor.AlternativeAuthor김형수-
dc.contributor.AlternativeAuthor김철우-
dc.identifier.doi10.1038/sj.onc.1208282-
Appears in Collections:
College of Medicine/School of Medicine (의과대학/대학원)Pathology (병리학전공)Journal Papers (저널논문_병리학전공)
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