当前位置： SCI文献检索 > JOURNAL OF CELLULAR BIOCHEMISTRY期刊下所有文献 > Superinduction of IL-6 by cycloheximide is associated with mRNA stabilization and sustained activation of p38 map kinase and NF-kappaB in cultured caco-2 cells.

Superinduction of IL-6 by cycloheximide is associated with mRNA stabilization and sustained activation of p38 map kinase and NF-kappaB in cultured caco-2 cells.

Abstract：

:Protein synthesis inhibitors paradoxically increase the expression of early-gene products, including various cytokines, through a process known as superinduction. Superinduction is cell-specific and the mechanisms involved are not fully understood but are usually attributed to decreased mRNA degradation. There is, however, increasing evidence that activation of signaling cascades and increased transcriptional activation may be involved as well. Recent studies suggest that IL-6 production in the intestinal mucosa is particularly important due to its anti-inflammatory and protective effects. The effect of protein synthesis inhibitors on IL-6 production in enterocytes, however, is unknown. Treatment of Caco-2 cells with cycloheximide (10 microg/ml) increased IL-6 mRNA and protein levels in IL-1beta-treated cells and this was associated with increased mRNA stabilization. In addition, cycloheximide suppressed IkappaBalpha resynthesis and prolonged p38MAP kinase activation and these changes were associated with sustained activation of the transcription factor NF-kappaB. NF-kappaB activation, in turn, was prevented by the specific p38MAP kinase inhibitor SB208350. Our results suggest that superinduction of IL-6 by cycloheximide in enterocytes results from both increased mRNA stabilization and upregulated transcriptional activity mediated by prolonged activation of the p38 MAP kinase and NF-kappaB.

journal_name

J Cell Biochem

journal_title

Journal of cellular biochemistry

authors

Hershko DD,Robb BW,Wray CJ,Luo GJ,Hasselgren PO

doi

10.1002/jcb.20014

subject

Has Abstract

pub_date

2004-04-01 00:00:00

pages

951-61

issue

5

eissn

0730-2312

issn

1097-4644

journal_volume

91

pub_type

杂志文章

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