| PGE2 confers survivin-dependent apoptosis resistance in human monocyte-derived dendritic cells. | |
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MedLine Citation:
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PMID: 15908458 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Control of apoptosis is fundamental for dendritic cell (DC) homeostasis. Numerous factors maintain DC viability throughout their lifespan, including inhibitor of apoptosis proteins. Among them, survivin is overexpressed in many human malignancies, but its physiological function in normal cells has not been fully delineated. Prostaglandin E2 (PGE2), also overproduced in several malignancies, has shown to induce proapoptotic and antiapoptotic effects in different cell types, including immune cells. In DC, PGE2 predominantly affects maturation and modulates immune functions. Here, we show that exposure of monocyte-derived DC to PGE2 (10(-5) M) for 72 h significantly increased DC survivin mRNA and protein expression. In contrast, DC, matured with lipopolysaccharide or tumor necrosis factor alpha, did not reveal survivin induction in response to PGE2. Following exposure to apoptotic stimuli, DC treated with PGE2 exhibited an overall increased viability compared with control DC, and this effect was correlated inversely with caspase-3 activation. Moreover, PGE2-treated, survivin-deficient DC demonstrated reduced viability in response to apoptotic stimuli. Further analysis indicated that PGE2 induced DC survivin expression in an E prostanoid (EP)2/EP4 receptor and phosphatidylinositol-3 kinase-dependent manner. These findings suggest that PGE2-dependent regulation of survivin is important in modulating apoptosis resistance in human DC. |
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Authors:
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Felicita Baratelli; Kostyantyn Krysan; Nathalie Heuzé-Vourc'h; Li Zhu; Brian Escuadro; Sherven Sharma; Karen Reckamp; Mariam Dohadwala; Steven M Dubinett |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S. Date: 2005-05-20 |
Journal Detail:
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Title: Journal of leukocyte biology Volume: 78 ISSN: 0741-5400 ISO Abbreviation: J. Leukoc. Biol. Publication Date: 2005 Aug |
Date Detail:
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Created Date: 2005-07-29 Completed Date: 2005-10-06 Revised Date: 2009-12-18 |
Medline Journal Info:
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Nlm Unique ID: 8405628 Medline TA: J Leukoc Biol Country: United States |
Other Details:
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Languages: eng Pagination: 555-64 Citation Subset: IM |
Affiliation:
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Jonsson Comprehensive Cancer Center and Division of Pulmonary and Critical Care Medicine, UCLA Geffen School of Medicine, 37-131 CHS, 10833 Le Conte Ave., Room 37-131 CHS, Los Angeles, CA 90095, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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1-Phosphatidylinositol 3-Kinase
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metabolism Apoptosis / drug effects*, radiation effects Caspase 3 Caspases / metabolism Cell Differentiation / drug effects*, physiology Cell Survival / drug effects, physiology Cells, Cultured Dendritic Cells / metabolism* Dinoprostone / metabolism, pharmacology* Enzyme Activation / drug effects, physiology Gene Expression Regulation / drug effects*, physiology Homeostasis / drug effects, physiology Humans Immunity, Cellular / drug effects, physiology Lipopolysaccharides / pharmacology Microtubule-Associated Proteins / metabolism* Monocytes / metabolism Neoplasm Proteins / metabolism* RNA, Messenger / biosynthesis Receptors, Prostaglandin E / metabolism Tumor Necrosis Factor-alpha / pharmacology |
| Grant Support | |
ID/Acronym/Agency:
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AI-28697/AI/NIAID NIH HHS; CA-16042/CA/NCI NIH HHS; P50 CA 90388/CA/NCI NIH HHS; R01 CA85686/CA/NCI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/BIRC5 protein, human; 0/Lipopolysaccharides; 0/Microtubule-Associated Proteins; 0/Neoplasm Proteins; 0/RNA, Messenger; 0/Receptors, Prostaglandin E; 0/Tumor Necrosis Factor-alpha; 0/prostaglandin E2 receptor, EP4 subtype; 0/prostaglandin EP2 receptor; 363-24-6/Dinoprostone; EC 2.7.1.137/1-Phosphatidylinositol 3-Kinase; EC 3.4.22.-/CASP3 protein, human; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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