Linked Life Data

8683110

Source:http://linkedlifedata.com/resource/pubmed/id/8683110

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1996-8-16
pubmed:abstractText
Sublethal levels of oxidative stress are well known to alter T cell functional responses, but the underlying mechanisms are unknown. The current study examined the effects of oxidative stress on transcriptional activities mediated by c-Fos/c-Jun AP-1 and the nuclear factor of activated T cells (NF-AT). The present results show that Jurkat T cells acutely exposed to micromolar concentrations of H2O2 exhibit substantial increases in AP-1 binding activity and the expression of c-jun but not c-fos mRNA. The preferential induction of c-jun by H2O2 did not represent redox stabilization of mRNA transcripts, and oxidative signals closely resembled PHA/PMA stimulation by effectively transactivating the full length c-jun promoter via the proximal jun1 tumor promoter-responsive element (TRE)-like promoter element. Similarly, the complexes binding the consensus AP-1 TRE and jun TRE-like motifs in cells exposed to oxidative signals or PHA/PMA were indistinguishable, being composed of c-Fos, c-Jun, and JunD. However, PHA/PMA but not oxidative signals induced the coordinate activation of reporter constructs containing the AP-1-TRE, NF-AT, and IL-2 promoter regions along with IL-2 mRNA expression. Furthermore, sublethal levels of H2O2 actively suppressed the transcriptional activation of NF-AT and IL-2 reporters as well as the expression of IL-2 mRNA in cells stimulated with PHA/PMA. Gel shift analysis revealed that oxidative suppression of NF-AT represented inhibition in the early generation of NFAT complexes rather than the binding of preformed NF-AT complexes. These results suggest that oxidative signals can positively and negatively regulate T cell transcriptional events and that changes in cellular redox can uncouple AP-1 regulation of c-jun from transcriptional up-regulation of IL-2 via NF-AT.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
157
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
160-9
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:8683110-Base Sequence, pubmed-meshheading:8683110-DNA-Binding Proteins, pubmed-meshheading:8683110-Genes, jun, pubmed-meshheading:8683110-Humans, pubmed-meshheading:8683110-Hydrogen Peroxide, pubmed-meshheading:8683110-Interleukin-2, pubmed-meshheading:8683110-Lymphoma, T-Cell, pubmed-meshheading:8683110-Molecular Sequence Data, pubmed-meshheading:8683110-NFATC Transcription Factors, pubmed-meshheading:8683110-Nuclear Proteins, pubmed-meshheading:8683110-Oxidative Stress, pubmed-meshheading:8683110-Phytohemagglutinins, pubmed-meshheading:8683110-Promoter Regions, Genetic, pubmed-meshheading:8683110-RNA, Messenger, pubmed-meshheading:8683110-T-Lymphocytes, pubmed-meshheading:8683110-Tetradecanoylphorbol Acetate, pubmed-meshheading:8683110-Transcription Factor AP-1, pubmed-meshheading:8683110-Transcription Factors, pubmed-meshheading:8683110-Transcriptional Activation, pubmed-meshheading:8683110-Tumor Cells, Cultured
pubmed:year
1996
pubmed:articleTitle
Sublethal levels of oxidative stress stimulate transcriptional activation of c-jun and suppress IL-2 promoter activation in Jurkat T cells.
pubmed:affiliation
Department of Medical Biochemistry, William H. Davis Medical Research Center, Ohio State University, Columbus 43210, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.