Source:http://linkedlifedata.com/resource/pubmed/id/20542496
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2010-7-27
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pubmed:abstractText |
Selenoprotein P (SeP), serving as selenium transporter and extracellular antioxidant, is assumed to have a protective role in the gastrointestinal tract, which is particularly susceptible to oxidative damage. Decreased SeP mRNA levels have been found in colon cancer; however, information on the control of intestinal SeP biosynthesis is scarce. We analyzed SeP biosynthesis in human intestinal epithelial Caco-2 cells subject to differentiation from crypt- to villous-like enterocytes. In the course of Caco-2 cell differentiation, SeP mRNA expression and secretion increased concomitant with three regulators of SeP transcription: hepatocyte nuclear factor-4alpha, forkhead box class O1a, and peroxisomal proliferator-activated receptor-gamma coactivator 1alpha. Treatment of differentiated Caco-2 cells with the proinflammatory cytokines IL-1beta, TNF-alpha, and IFN-gamma caused a down-regulation of SeP biosynthesis, resulting from induction of nitric oxide synthase 2. These observations were corroborated by decreased SeP mRNA levels in the colon of dextran sodium sulfate-treated mice, an animal model of experimental colitis. We conclude that inflammation of the intestinal mucosa causes a decline in locally produced selenoprotein P in the colon that eventually may contribute to the emergence of inflammatory bowel disease-related colorectal cancer.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Inflammation Mediators,
http://linkedlifedata.com/resource/pubmed/chemical/NOS2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type II,
http://linkedlifedata.com/resource/pubmed/chemical/Selenoprotein P
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1873-4596
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pubmed:author | |
pubmed:copyrightInfo |
Copyright 2010 Elsevier Inc. All rights reserved.
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pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
49
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
777-85
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pubmed:dateRevised |
2011-10-27
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pubmed:meshHeading |
pubmed-meshheading:20542496-Animals,
pubmed-meshheading:20542496-Caco-2 Cells,
pubmed-meshheading:20542496-Cell Differentiation,
pubmed-meshheading:20542496-Cell Line, Tumor,
pubmed-meshheading:20542496-Cytokines,
pubmed-meshheading:20542496-Down-Regulation,
pubmed-meshheading:20542496-Enzyme Induction,
pubmed-meshheading:20542496-Female,
pubmed-meshheading:20542496-Humans,
pubmed-meshheading:20542496-Inflammation Mediators,
pubmed-meshheading:20542496-Inflammatory Bowel Diseases,
pubmed-meshheading:20542496-Intestines,
pubmed-meshheading:20542496-Mice,
pubmed-meshheading:20542496-Mice, Inbred C57BL,
pubmed-meshheading:20542496-Nitric Oxide Synthase Type II,
pubmed-meshheading:20542496-Selenoprotein P
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pubmed:year |
2010
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pubmed:articleTitle |
Proinflammatory cytokines down-regulate intestinal selenoprotein P biosynthesis via NOS2 induction.
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pubmed:affiliation |
Institute for Biochemistry and Molecular Biology I, Heinrich-Heine University, D-40225 Düsseldorf, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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