Linked Life Data

15592513

Source:http://linkedlifedata.com/resource/pubmed/id/15592513

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2005-2-11
pubmed:abstractText
Many 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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1252-61
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15592513-Acetylcysteine, pubmed-meshheading:15592513-Antibodies, Monoclonal, pubmed-meshheading:15592513-Antigens, CD95, pubmed-meshheading:15592513-Antioxidants, pubmed-meshheading:15592513-Apoptosis, pubmed-meshheading:15592513-Cytochromes c, pubmed-meshheading:15592513-Gene Expression, pubmed-meshheading:15592513-Genes, bcl-2, pubmed-meshheading:15592513-Humans, pubmed-meshheading:15592513-Hydrogen Peroxide, pubmed-meshheading:15592513-Jurkat Cells, pubmed-meshheading:15592513-Mitochondria, pubmed-meshheading:15592513-NF-kappa B, pubmed-meshheading:15592513-Oxidative Stress, pubmed-meshheading:15592513-Proto-Oncogene Proteins c-bcl-2, pubmed-meshheading:15592513-Reactive Oxygen Species, pubmed-meshheading:15592513-T-Lymphocytes, pubmed-meshheading:15592513-Up-Regulation
pubmed:year
2005
pubmed:articleTitle
Oxidative stress attenuates Fas-mediated apoptosis in Jurkat T cell line through Bfl-1 induction.
pubmed:affiliation
Department of Pathology, Tumor Immunity Medical Research Center and Cancer Research Institute, Seoul National University College of Medicine, 28 Yongon-dong, Chongno-gu, Seoul 110-799, Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't