Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2007-9-21
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0006-3002
pubmed:author
pubmed:issnType
Print
pubmed:volume
1771
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1177-85
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
pubmed:year
2007
pubmed:articleTitle
Expression of the phospholipid scramblase (PLSCR) gene family during the acute phase response.
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
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural