Linked Life Data

16413748

Source:http://linkedlifedata.com/resource/pubmed/id/16413748

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2006-6-12
pubmed:abstractText
We have previously revealed that LPS can activate transcription of the IL-10 gene promoter through transcription factors Sp1, C/EBPbeta and C/EBPdelta in mouse macrophages. In this study, we determined that NF-kappaB 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-kappaB 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 IkappaB 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/EBPbeta and delta could activate IL-10 gene expression. In this study, we also identified that all four pharmacological inhibitors inhibited the protein expression of C/EBPdelta individually, but not C/EBPbeta. In the presence of all three MAPK inhibitors, or only NF-kappaB inhibitor, LPS-induced protein expression and DNA binding of C/EBPdelta 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-kappaB- and MAPK-induced protein expression and DNA binding of C/EBPdelta.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0898-6568
pubmed:author
pubmed:issnType
Print
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1492-500
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:16413748-Animals, pubmed-meshheading:16413748-CCAAT-Enhancer-Binding Protein-beta, pubmed-meshheading:16413748-CCAAT-Enhancer-Binding Protein-delta, pubmed-meshheading:16413748-Cell Line, pubmed-meshheading:16413748-Dose-Response Relationship, Drug, pubmed-meshheading:16413748-Enzyme Activation, pubmed-meshheading:16413748-Genes, Reporter, pubmed-meshheading:16413748-Interleukin-10, pubmed-meshheading:16413748-Lipopolysaccharides, pubmed-meshheading:16413748-MAP Kinase Signaling System, pubmed-meshheading:16413748-Macrophages, pubmed-meshheading:16413748-Mice, pubmed-meshheading:16413748-Mitogen-Activated Protein Kinases, pubmed-meshheading:16413748-NF-kappa B, pubmed-meshheading:16413748-Promoter Regions, Genetic, pubmed-meshheading:16413748-Protein Kinase Inhibitors, pubmed-meshheading:16413748-Transcriptional Activation
pubmed:year
2006
pubmed:articleTitle
Lipopolysaccharide-induced transcriptional activation of interleukin-10 is mediated by MAPK- and NF-kappaB-induced CCAAT/enhancer-binding protein delta in mouse macrophages.
pubmed:affiliation
Graduate Institute of Biopharmaceutics, College of Life Sciences, National Chiayi University, Chiayi, Taiwan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't