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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1994-7-25
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pubmed:abstractText |
Lipopolysaccharide (LPS)-induced phospholipase D (PLD) activation was investigated in undifferentiated monocytic leukemic cell lines THP-1 and U-937. Treatment of THP-1 or U-937 cells labelled with [32P]orthophosphate, [32P]acyl GPC or [3H]alkyl GPC with LPS, in the presence of 0.5% ethanol, resulted in the accumulation of labelled phosphatidylethanol (PEt) through PLD activation. LPS-mediated PLD activation of THP-1 or U-937 was inhibited by staurosporine (2 microM) and by protein kinase C (PKC) down-regulation with 12-O-tetradecanoylphorbol 13-acetate (TPA) suggesting a role for PKC. In addition to LPS, TPA, ionomycin and cell-permeant analogs of diacylglycerol also stimulated [3H]PEt accumulation. The TPA-induced PEt accumulation was also completely abolished by staurosporine or down-regulation of PKC (> 95% inhibition). Furthermore, the LPS-mediated [32P]PEt formation was attenuated by either depletion of extracellular Ca2+ with EGTA (5 mM) or chelation of intracellular Ca2+ by BAPTA (30 microM). These results indicate that an increase in intracellular Ca2+ is necessary for LPS-mediated PLD activation. Further support for PKC activation by LPS was obtained by determining PKC activity in an in vitro assay of histone H1 phosphorylation using [gamma-32P]ATP. In untreated THP-1 cells, approximately 64% of the PKC activity was localized in the cytosol and 36% in the membrane fraction. Treatment of the cells with LPS (10 micrograms/ml, for 2 h) resulted in an increase of 10% of the membrane-associated PKC activity and a corresponding decrease in the cytosol fraction. These data provide evidence that one of the mechanisms of LPS-mediated signal transduction in human monocytic cell lines involves activation of PLD.
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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/1,2-diacylglycerol,
http://linkedlifedata.com/resource/pubmed/chemical/Alkaloids,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Diglycerides,
http://linkedlifedata.com/resource/pubmed/chemical/Glycerophospholipids,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphatidic Acids,
http://linkedlifedata.com/resource/pubmed/chemical/Phospholipase D,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C,
http://linkedlifedata.com/resource/pubmed/chemical/Staurosporine,
http://linkedlifedata.com/resource/pubmed/chemical/Tetradecanoylphorbol Acetate,
http://linkedlifedata.com/resource/pubmed/chemical/phosphatidylethanol
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0006-3002
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
23
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pubmed:volume |
1213
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
14-20
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:8011674-Alkaloids,
pubmed-meshheading:8011674-Calcium,
pubmed-meshheading:8011674-Diglycerides,
pubmed-meshheading:8011674-Enzyme Activation,
pubmed-meshheading:8011674-Glycerophospholipids,
pubmed-meshheading:8011674-Humans,
pubmed-meshheading:8011674-Lipopolysaccharides,
pubmed-meshheading:8011674-Phosphatidic Acids,
pubmed-meshheading:8011674-Phospholipase D,
pubmed-meshheading:8011674-Protein Kinase C,
pubmed-meshheading:8011674-Signal Transduction,
pubmed-meshheading:8011674-Staurosporine,
pubmed-meshheading:8011674-Tetradecanoylphorbol Acetate,
pubmed-meshheading:8011674-Tumor Cells, Cultured
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pubmed:year |
1994
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pubmed:articleTitle |
Lipopolysaccharide-mediated signal transduction through phospholipase D activation in monocytic cell lines.
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pubmed:affiliation |
Department of Medicine, Indiana University School of Medicine, Indianapolis 46202.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
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