Peptidoglycan enhances transcriptional expression of CCAAT/enhancer-binding protein delta gene in mouse macrophages.

Yu Chiuan Huang, Wen Chang Chang, Jyan Gwo J Su, Jheng Liang Cai, Chun Chia Chen, Jan Jong Hung, Yi Wen Liu

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Peptidoglycan-activated gene expression is mediated through various transcription factors including CCAAT/enhancer-binding protein delta (C/EBPdelta). The purpose of the present study is to elucidate the mechanism of PGN-activated C/EBPdelta gene. PGN stimulated C/EBPdelta protein and mRNA expression in mouse macrophages RAW 264.7 cells. Analysis of C/EBPdelta promoter activity by luciferase reporter assay indicated that PGN-induced C/EBPdelta gene activation is partially mediated by the -345 to +24 bp of C/EBPdelta gene promoter. The in vitro protein-DNA binding assay showed that Sp1, c-Rel and c-Jun are the major protein binding to this PGN-response element of C/EBPdelta promoter, and the binding of c-Rel and c-Jun is increased after PGN treatment. All of these binding activities were abolished when Sp1-, NF-kappaB/APRE-, CRE-sites were mutated. Furthermore, analysis of this promoter region by site-directed mutants constructed in luciferase reporter vector indicated that two Sp1-sites, one NF-kappaB/APRE-site and one CRE-site are prominent for PGN-induced gene expression. In addition, when Sp1, c-Rel or c-Jun transcription factors were overexpressed in cells, all of them enhanced C/EBPdelta promoter activity. In summary, we suggest that Sp1, c-Rel and c-Jun transcription factors play important roles in activation of C/EBPdelta gene promoter under the stimulation of PGN. Given the importance of C/EBPdelta in inflammatory disease, these results reveal a clue as a potential therapeutic target for suppression of C/EBPdelta expression under PGN stimulation.

Original languageEnglish
Pages (from-to)407-418
Number of pages12
JournalJournal of Biomedical Science
Volume14
Issue number3
DOIs
Publication statusPublished - May 2007
Externally publishedYes

Fingerprint

CCAAT-Enhancer-Binding Protein-delta
Peptidoglycan
Macrophages
Genes
Transcription Factors
NF-kappa B
Luciferases
Gene expression
Assays
Chemical activation
Proto-Oncogene Proteins c-jun
Gene Expression
DNA-Binding Proteins
Response Elements
Genetic Promoter Regions
Protein Binding

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Peptidoglycan enhances transcriptional expression of CCAAT/enhancer-binding protein delta gene in mouse macrophages. / Huang, Yu Chiuan; Chang, Wen Chang; Su, Jyan Gwo J; Cai, Jheng Liang; Chen, Chun Chia; Hung, Jan Jong; Liu, Yi Wen.

In: Journal of Biomedical Science, Vol. 14, No. 3, 05.2007, p. 407-418.

Research output: Contribution to journalArticle

Huang, Yu Chiuan ; Chang, Wen Chang ; Su, Jyan Gwo J ; Cai, Jheng Liang ; Chen, Chun Chia ; Hung, Jan Jong ; Liu, Yi Wen. / Peptidoglycan enhances transcriptional expression of CCAAT/enhancer-binding protein delta gene in mouse macrophages. In: Journal of Biomedical Science. 2007 ; Vol. 14, No. 3. pp. 407-418.
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abstract = "Peptidoglycan-activated gene expression is mediated through various transcription factors including CCAAT/enhancer-binding protein delta (C/EBPdelta). The purpose of the present study is to elucidate the mechanism of PGN-activated C/EBPdelta gene. PGN stimulated C/EBPdelta protein and mRNA expression in mouse macrophages RAW 264.7 cells. Analysis of C/EBPdelta promoter activity by luciferase reporter assay indicated that PGN-induced C/EBPdelta gene activation is partially mediated by the -345 to +24 bp of C/EBPdelta gene promoter. The in vitro protein-DNA binding assay showed that Sp1, c-Rel and c-Jun are the major protein binding to this PGN-response element of C/EBPdelta promoter, and the binding of c-Rel and c-Jun is increased after PGN treatment. All of these binding activities were abolished when Sp1-, NF-kappaB/APRE-, CRE-sites were mutated. Furthermore, analysis of this promoter region by site-directed mutants constructed in luciferase reporter vector indicated that two Sp1-sites, one NF-kappaB/APRE-site and one CRE-site are prominent for PGN-induced gene expression. In addition, when Sp1, c-Rel or c-Jun transcription factors were overexpressed in cells, all of them enhanced C/EBPdelta promoter activity. In summary, we suggest that Sp1, c-Rel and c-Jun transcription factors play important roles in activation of C/EBPdelta gene promoter under the stimulation of PGN. Given the importance of C/EBPdelta in inflammatory disease, these results reveal a clue as a potential therapeutic target for suppression of C/EBPdelta expression under PGN stimulation.",
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