Dexamethasone inhibits IL-1β gene expression in LPS-stimulated RAW 264.7 cells by blocking NF-κB/Rel and AP-1 activation

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dc.contributor.authorYoung Jin Jeon-
dc.contributor.authorSeung H Han-
dc.contributor.authorYong W Lee-
dc.contributor.authorMichael Lee-
dc.contributor.authorKyu H Yang-
dc.contributor.authorHwan Mook Kim-
dc.date.accessioned2017-04-19T08:57:15Z-
dc.date.available2017-04-19T08:57:15Z-
dc.date.issued2000-
dc.identifier.issn0162-3109-
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/5170-
dc.description.abstractIn the present study, the mechanism by which dexamethasone (DEX) inhibited IL-1β gene expression in bacterial lipopolysaccharide (LPS)-activated RAW 264.7 cells was investigated. The decrease in LPS-induced IL-1β mRNA expression was demonstrated by quantitative reverse transcription polymerase chain reaction (RT-PCR). Since the promoter in IL-1β gene contains binding motifs for NF-κB/Rel, AP-1, NF-IL6, and CREB/ATF, which appear to be important in LPS-mediated IL-1β induction, the effects of DEX on the activation of these transcription factors were examined. Treatment of DEX to RAW 264.7 cells induced a dose-related inhibition of NF-κB/Rel and AP-1 in chloramphenicol acetyltransferase activity, while neither NF-IL6 nor CREB/ATF activation was affected by DEX. Treatment of RAW 264.7 cells with DEX inhibited DNA binding of NF-κB/Rel and AP-1 proteins to their cognate DNA sites as measured by electrophoretic mobility shift assay (EMSA). DEX treatment caused a significant reduction in nuclear c-rel, p65, and p50 protein contents, and these decreases were paralleled by the accumulation of cytoplasmic c-rel, p65, and p50. DEX treatment of RAW 264.7 cells did not inhibit the nuclear translocation of c-jun and c-fos. We found that the inhibition of IL-1β production by DEX is not related to p38, which is important in the IL-1β induction. These results suggest that DEX may inhibit IL-1β gene expression by a mechanism involving the blocking of LPS-induced NF-κB/Rel and AP-1 activation.-
dc.publisherElsevier-
dc.titleDexamethasone inhibits IL-1β gene expression in LPS-stimulated RAW 264.7 cells by blocking NF-κB/Rel and AP-1 activation-
dc.title.alternativeDexamethasone inhibits IL-1β gene expression in LPS-stimulated RAW 264.7 cells by blocking NF-κB/Rel and AP-1 activation-
dc.typeArticle-
dc.citation.titleImmunopharmacology-
dc.citation.number2-
dc.citation.endPage183-
dc.citation.startPage173-
dc.citation.volume48-
dc.contributor.affiliatedAuthorYoung Jin Jeon-
dc.contributor.affiliatedAuthorSeung H Han-
dc.contributor.affiliatedAuthorMichael Lee-
dc.contributor.affiliatedAuthorHwan Mook Kim-
dc.contributor.alternativeName전영진-
dc.contributor.alternativeName한승현-
dc.contributor.alternativeName이용우-
dc.contributor.alternativeName이미가엘-
dc.contributor.alternativeName양규환-
dc.contributor.alternativeName김환묵-
dc.identifier.bibliographicCitationImmunopharmacology, vol. 48, no. 2, pp. 173-183-
dc.identifier.doi10.1016/S0162-3109(00)00199-5-
dc.subject.keyworddexamethasone-
dc.subject.keywordIL-1β-
dc.subject.keywordNF-κB/Rel-
dc.subject.keywordAP-1-
dc.subject.keywordglucocorticoid receptor-
dc.subject.localdexamethasone-
dc.subject.localDexamethasone-
dc.subject.localIL-1β-
dc.subject.localNF-κB/Rel-
dc.subject.localAP-1-
dc.subject.localglucocorticoid receptor-
dc.description.journalClassY-
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