Source:http://linkedlifedata.com/resource/pubmed/id/17590392
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
9
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pubmed:dateCreated |
2007-9-21
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pubmed:abstractText |
Phospholipid scramblase 1 (PLSCR1) is a member of PLSCR gene family that has been implicated in multiple cellular processes including movement of phospholipids, gene regulation, immuno-activation, and cell proliferation/apoptosis. In the present study, we identified PLSCR1 as a positive intracellular acute phase protein that is upregulated by LPS in liver, heart, and adipose tissue, but not skeletal muscle. LPS administration resulted in a marked increase in PLSCR1 mRNA and protein levels in the liver. This stimulation occurred rapidly (within 2 h), and was very sensitive to LPS (half-maximal response at 0.1 microg/mouse). Moreover, two other APR-inducers, zymosan and turpentine, also produced significant increases in PLSCR1 mRNA and protein levels, indicating that PLSCR1 was stimulated in a number of models of the APR. To determine signaling pathways by which LPS stimulated PLSCR1, we examined the effect of proinflammatory cytokines in vitro and in vivo. TNFalpha, IL-1beta, and IL-6 all stimulated PLSCR1 in cultured Hep B3 hepatocytes, whereas only TNFalpha stimulated PLSCR1 in cultured 3T3-L1 adipocytes, suggesting cell type-specific effects of cytokines. Furthermore, the LPS-stimulated increase in liver PLSCR1 mRNA was greatly attenuated by 80% in TNFalpha and IL-1beta receptor null mice as compared to wild-type controls. In contrast, PLSCR1 levels in adipose tissue were induced to a similar extent in TNFalpha and IL-1beta receptor null mice and controls. These results indicate that maximal stimulation of PLSCR1 by LPS in liver required TNFalpha and/or IL-1beta, whereas the stimulation of PLSCR1 in adipose tissue is not dependent on TNFalpha and/or IL-1beta. These data provide evidence that PLSCR1 is a positive intracellular acute phase protein with a tissue-specific mechanism for up-regulation.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1beta,
http://linkedlifedata.com/resource/pubmed/chemical/Isoenzymes,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Phospholipid Transfer Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Plscr1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Solvents,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/Turpentine,
http://linkedlifedata.com/resource/pubmed/chemical/Zymosan
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0006-3002
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
1771
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1177-85
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pubmed:meshHeading |
pubmed-meshheading:17590392-3T3-L1 Cells,
pubmed-meshheading:17590392-Acute-Phase Reaction,
pubmed-meshheading:17590392-Adipose Tissue,
pubmed-meshheading:17590392-Animals,
pubmed-meshheading:17590392-Enzyme Induction,
pubmed-meshheading:17590392-Female,
pubmed-meshheading:17590392-Genes, Immediate-Early,
pubmed-meshheading:17590392-Humans,
pubmed-meshheading:17590392-Interleukin-1beta,
pubmed-meshheading:17590392-Isoenzymes,
pubmed-meshheading:17590392-Lipopolysaccharides,
pubmed-meshheading:17590392-Liver,
pubmed-meshheading:17590392-Mice,
pubmed-meshheading:17590392-Mice, Inbred C57BL,
pubmed-meshheading:17590392-Mice, Knockout,
pubmed-meshheading:17590392-Multigene Family,
pubmed-meshheading:17590392-Muscle, Skeletal,
pubmed-meshheading:17590392-Myocardium,
pubmed-meshheading:17590392-Phospholipid Transfer Proteins,
pubmed-meshheading:17590392-Solvents,
pubmed-meshheading:17590392-Tumor Necrosis Factor-alpha,
pubmed-meshheading:17590392-Turpentine,
pubmed-meshheading:17590392-Zymosan
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pubmed:year |
2007
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pubmed:articleTitle |
Expression of the phospholipid scramblase (PLSCR) gene family during the acute phase response.
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pubmed:affiliation |
Metabolism Section, Department of Veterans Affairs Medical Center, University of California San Francisco, 4150 Clement Street, San Francisco, CA 94121, USA. lubiao@gmail.com
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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