Abstract:
:We investigated the mechanisms by which the heat shock response inhibits inducible nitric oxide synthase (iNOS) gene expression. Incubation of cultured murine lung epithelium (MLE-15) at temperatures ranging from 39 to 43 degrees C, for 1 h, demonstrated that only severe thermal stress (41 to 43 degrees C) was sufficient to induce the heat shock response. Thermal stress inhibited cytokine-mediated iNOS gene expression only when associated with induction of the heat shock response. Transient transfection assays with an iNOS promoter-reporter gene construct demonstrated that the heat shock response inhibited cytokine-mediated iNOS promoter activity. Electromobility gel shift assays demonstrated that the heat shock response inhibited cytokine-mediated NF-kappa B nuclear translocation. The heat shock response also inhibited cytokine-mediated I kappa-B degradation. These data suggest that the heat shock response inhibits iNOS gene expression by transcriptional mechanisms involving the NF-kappa B/ I kappa-B pathway.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Wong HR,Ryan M,Wispé JRdoi
10.1006/bbrc.1997.6076subject
Has Abstractpub_date
1997-02-13 00:00:00pages
257-63issue
2eissn
0006-291Xissn
1090-2104pii
S0006-291X(97)96076-9journal_volume
231pub_type
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journal_title:Biochemical and biophysical research communications
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journal_title:Biochemical and biophysical research communications
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journal_title:Biochemical and biophysical research communications
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journal_title:Biochemical and biophysical research communications
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journal_title:Biochemical and biophysical research communications
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journal_title:Biochemical and biophysical research communications
pub_type: 杂志文章
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journal_title:Biochemical and biophysical research communications
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journal_title:Biochemical and biophysical research communications
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