NDLI: Regulation of interleukin-8 gene at a distinct site of its promoter by CCAAT enhancer-binding protein homologous protein in prostaglandin E2-treated human T cells.

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Regulation of interleukin-8 gene at a distinct site of its promoter by CCAAT enhancer-binding protein homologous protein in prostaglandin E2-treated human T cells.

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Regulation of interleukin-8 gene at a distinct site of its promoter by CCAAT enhancer-binding protein homologous protein in prostaglandin E2-treated human T cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Aguennouz, Mohamed Cucinotta, Maria Altucci, Lucia Valenti, Andrea Loddo, Saverio Visalli, Maria Teti, Diana
Description	Author Affiliation: Cucinotta M ( Department of Experimental Pathology and Microbiology, University of Messina, Messina 98100, Italy.)
Abstract	For a long period of time, the transcription factor CCAAT/enhancer-binding protein homologous protein (CHOP) has been thought to inhibit transcriptional activity for its ability to interact with CCAAT enhancer-binding protein family factors, thus preventing their binding to DNA. We have previously shown that in human T lymphocytes the CHOP phosphorylation induced by prostaglandin E(2) (PGE(2))-increased interleukin-8 (IL-8) gene expression. Given the CHOP positive role in the regulation of transcription, here we have investigated the molecular mechanism(s) by which CHOP increases IL-8 gene activity under PGE(2) stimulus. Transfection experiments with mutants showed both that the CHOP transactivation domain is essential for IL-8 transcription and that the IL-8/activator protein 1 (AP-1) promoter mutated in NF-kappaB and NF-IL-6, but not in the AP-1 site, harbors essential CHOP-responsive elements. CHOP silencing confirmed its role in the IL-8 transcriptional regulation and protein production, whereas c-Jun small interfering RNA experiments showed that the PGE(2)-induced activation of IL-8 promoter is mainly c-Jun-independent. Moreover, PGE(2) induced CHOP-DNA complexes only when the entire IL-8/AP-1 promoter or the wild type sequences encompassing the AP-1 upstream region were employed. Mutations introduced in these sequences prevented the DNA-CHOP complex formation. The IL-8/AP-1 mutant promoter lacking the sequence immediately upstream the AP-1 site is PGE(2)-unresponsive. Finally, chromatin immunoprecipitation data confirmed in vivo that PGE(2) induces CHOP binding to the IL-8 promoter. Taken together, our results suggest that the increased expression of CHOP in response to PGE(2) exerts a positive transcriptional regulation of the IL-8 promoter mediated by direct binding to a novel consensus site.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	44
Volume Number	283
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2008-10-31
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Dinoprostone Metabolism Gene Expression Regulation Interleukin-8 Biosynthesis Genetics Promoter Regions, Genetic T-Lymphocytes Binding Sites CCAAT-Enhancer-Binding Proteins Enhancer Elements, Genetic Jurkat Cells Molecular Sequence Data Mutation Transcription Factor AP-1 Transcription Factor CHOP Research Support, Non-U.S. Gov't Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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