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

Research output: Contribution to journalArticle

80 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)1492-1500
Number of pages9
JournalCellular Signalling
Volume18
Issue number9
DOIs
Publication statusPublished - Sep 2006
Externally publishedYes

Fingerprint

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

Keywords

  • C/EBPδ
  • Interleukin-10
  • LPS
  • MAPK
  • NF-κB

ASJC Scopus subject areas

  • Cell Biology

Cite this

Lipopolysaccharide-induced transcriptional activation of interleukin-10 is mediated by MAPK- and NF-κB-induced CCAAT/enhancer-binding protein δ in mouse macrophages. / Liu, Yi Wen; Chen, Chun Chia; Tseng, Hui Ping; Chang, Wen Chang.

In: Cellular Signalling, Vol. 18, No. 9, 09.2006, p. 1492-1500.

Research output: Contribution to journalArticle

@article{d3c293421d56447d9f0a17ebf8030f45,
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}",
year = "2006",
month = "9",
doi = "10.1016/j.cellsig.2005.12.001",
language = "English",
volume = "18",
pages = "1492--1500",
journal = "Cellular Signalling",
issn = "0898-6568",
publisher = "Elsevier Inc.",
number = "9",

}

TY - JOUR

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

UR - http://www.scopus.com/inward/record.url?scp=33744783446&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33744783446&partnerID=8YFLogxK

U2 - 10.1016/j.cellsig.2005.12.001

DO - 10.1016/j.cellsig.2005.12.001

M3 - Article

C2 - 16413748

AN - SCOPUS:33744783446

VL - 18

SP - 1492

EP - 1500

JO - Cellular Signalling

JF - Cellular Signalling

SN - 0898-6568

IS - 9

ER -