Lipopolysaccharide-induced transcriptional activation of interleukin-10 is mediated by MAPK- and NF-κB-induced CCAAT/enhancer-binding protein δ in mouse macrophages

Yi Wen Liu, Chun Chia Chen, Hui Ping Tseng, Wen Chang Chang

研究成果: 雜誌貢獻文章

81 引文 (Scopus)

摘要

We have previously revealed that LPS can activate transcription of the IL-10 gene promoter through transcription factors Sp1, C/EBPβ and C/EBPδ in mouse macrophages. In this study, we determined that NF-κB and MAPK signal pathways, including ERK, JNK, and p38, were all involved in LPS-induced IL-10 gene expression. Treatment of cells with the pharmacological inhibitors of ERK, JNK, p38 and NF-κB respectively inhibited LPS-induced IL-10 protein expression in a dose-dependent manner. These inhibitors also decreased the LPS-induced IL-10 mRNA expression at a high concentration used. With transient overexpression of the IκB expression plasmids, or the dominant negative plasmids of ERK2, JNK, p38 together with reporter vector containing IL-10 promoter region, all four expression plasmids inhibited LPS-induced IL-10 promoter activity individually. It is known that the increase in protein and DNA binding of C/EBPβ and δ could activate IL-10 gene expression. In this study, we also identified that all four pharmacological inhibitors inhibited the protein expression of C/EBPδ individually, but not C/EBPβ. In the presence of all three MAPK inhibitors, or only NF-κB inhibitor, LPS-induced protein expression and DNA binding of C/EBPδ were completely inhibited simultaneously, and LPS-induced expression of IL-10 protein and mRNA was also inhibited totally. Taken together, these results suggested that LPS-induced IL-10 expression was mediated at least through the pathway of NF-κB- and MAPK-induced protein expression and DNA binding of C/EBPδ.

原文英語
頁(從 - 到)1492-1500
頁數9
期刊Cellular Signalling
18
發行號9
DOIs
出版狀態已發佈 - 九月 2006
對外發佈Yes

指紋

CCAAT-Enhancer-Binding Proteins
Interleukin-10
Transcriptional Activation
Lipopolysaccharides
Macrophages
DNA-Binding Proteins
Plasmids
Pharmacology
Sp1 Transcription Factor
Gene Expression
Messenger RNA
Genetic Promoter Regions
Signal Transduction
Proteins

ASJC Scopus subject areas

  • Cell Biology

引用此文

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title = "Lipopolysaccharide-induced transcriptional activation of interleukin-10 is mediated by MAPK- and NF-κB-induced CCAAT/enhancer-binding protein δ in mouse macrophages",
abstract = "We have previously revealed that LPS can activate transcription of the IL-10 gene promoter through transcription factors Sp1, C/EBPβ and C/EBPδ in mouse macrophages. In this study, we determined that NF-κB and MAPK signal pathways, including ERK, JNK, and p38, were all involved in LPS-induced IL-10 gene expression. Treatment of cells with the pharmacological inhibitors of ERK, JNK, p38 and NF-κB respectively inhibited LPS-induced IL-10 protein expression in a dose-dependent manner. These inhibitors also decreased the LPS-induced IL-10 mRNA expression at a high concentration used. With transient overexpression of the IκB expression plasmids, or the dominant negative plasmids of ERK2, JNK, p38 together with reporter vector containing IL-10 promoter region, all four expression plasmids inhibited LPS-induced IL-10 promoter activity individually. It is known that the increase in protein and DNA binding of C/EBPβ and δ could activate IL-10 gene expression. In this study, we also identified that all four pharmacological inhibitors inhibited the protein expression of C/EBPδ individually, but not C/EBPβ. In the presence of all three MAPK inhibitors, or only NF-κB inhibitor, LPS-induced protein expression and DNA binding of C/EBPδ were completely inhibited simultaneously, and LPS-induced expression of IL-10 protein and mRNA was also inhibited totally. Taken together, these results suggested that LPS-induced IL-10 expression was mediated at least through the pathway of NF-κB- and MAPK-induced protein expression and DNA binding of C/EBPδ.",
keywords = "C/EBPδ, Interleukin-10, LPS, MAPK, NF-κB",
author = "Liu, {Yi Wen} and Chen, {Chun Chia} and Tseng, {Hui Ping} and Chang, {Wen Chang}",
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pages = "1492--1500",
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T1 - Lipopolysaccharide-induced transcriptional activation of interleukin-10 is mediated by MAPK- and NF-κB-induced CCAAT/enhancer-binding protein δ in mouse macrophages

AU - Liu, Yi Wen

AU - Chen, Chun Chia

AU - Tseng, Hui Ping

AU - Chang, Wen Chang

PY - 2006/9

Y1 - 2006/9

N2 - We have previously revealed that LPS can activate transcription of the IL-10 gene promoter through transcription factors Sp1, C/EBPβ and C/EBPδ in mouse macrophages. In this study, we determined that NF-κB and MAPK signal pathways, including ERK, JNK, and p38, were all involved in LPS-induced IL-10 gene expression. Treatment of cells with the pharmacological inhibitors of ERK, JNK, p38 and NF-κB respectively inhibited LPS-induced IL-10 protein expression in a dose-dependent manner. These inhibitors also decreased the LPS-induced IL-10 mRNA expression at a high concentration used. With transient overexpression of the IκB expression plasmids, or the dominant negative plasmids of ERK2, JNK, p38 together with reporter vector containing IL-10 promoter region, all four expression plasmids inhibited LPS-induced IL-10 promoter activity individually. It is known that the increase in protein and DNA binding of C/EBPβ and δ could activate IL-10 gene expression. In this study, we also identified that all four pharmacological inhibitors inhibited the protein expression of C/EBPδ individually, but not C/EBPβ. In the presence of all three MAPK inhibitors, or only NF-κB inhibitor, LPS-induced protein expression and DNA binding of C/EBPδ were completely inhibited simultaneously, and LPS-induced expression of IL-10 protein and mRNA was also inhibited totally. Taken together, these results suggested that LPS-induced IL-10 expression was mediated at least through the pathway of NF-κB- and MAPK-induced protein expression and DNA binding of C/EBPδ.

AB - We have previously revealed that LPS can activate transcription of the IL-10 gene promoter through transcription factors Sp1, C/EBPβ and C/EBPδ in mouse macrophages. In this study, we determined that NF-κB and MAPK signal pathways, including ERK, JNK, and p38, were all involved in LPS-induced IL-10 gene expression. Treatment of cells with the pharmacological inhibitors of ERK, JNK, p38 and NF-κB respectively inhibited LPS-induced IL-10 protein expression in a dose-dependent manner. These inhibitors also decreased the LPS-induced IL-10 mRNA expression at a high concentration used. With transient overexpression of the IκB expression plasmids, or the dominant negative plasmids of ERK2, JNK, p38 together with reporter vector containing IL-10 promoter region, all four expression plasmids inhibited LPS-induced IL-10 promoter activity individually. It is known that the increase in protein and DNA binding of C/EBPβ and δ could activate IL-10 gene expression. In this study, we also identified that all four pharmacological inhibitors inhibited the protein expression of C/EBPδ individually, but not C/EBPβ. In the presence of all three MAPK inhibitors, or only NF-κB inhibitor, LPS-induced protein expression and DNA binding of C/EBPδ were completely inhibited simultaneously, and LPS-induced expression of IL-10 protein and mRNA was also inhibited totally. Taken together, these results suggested that LPS-induced IL-10 expression was mediated at least through the pathway of NF-κB- and MAPK-induced protein expression and DNA binding of C/EBPδ.

KW - C/EBPδ

KW - Interleukin-10

KW - LPS

KW - MAPK

KW - NF-κB

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