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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1 Pt 1
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pubmed:dateCreated |
1998-2-19
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pubmed:abstractText |
Previously we have shown that hyperosmolarity increases Na(+)-myo-inositol cotransporter (SMIT) activity and mRNA levels in cultured endothelial cells. Because hyperosmolarity and cytokines, such as tumor necrosis factor-alpha (TNF-alpha), activate similar signal transduction pathways, we examined the effect of TNF-alpha on SMIT mRNA levels and myo-inositol accumulation. In contrast to the effect of hyperosmolarity, TNF-alpha caused a time- and concentration-dependent decrease in SMIT mRNA levels and myo-inositol accumulation. The effect of TNF-alpha on myo-inositol accumulation was found in large-vessel endothelial cells (derived from the aorta and pulmonary artery) and cerebral microvessel endothelial cells. In bovine aorta and bovine pulmonary artery endothelial cells, TNF-alpha activated nuclear factor (NF)-kappa B. TNF-alpha also increased ceramide levels, and C2-ceramide mimicked the effect of TNF-alpha on SMIT mRNA levels and myo-inositol accumulation in bovine aorta endothelial cells. Pyrrolidinedithiocarbamate, genistein, and 7-amino-1-chloro-3-tosylamido-2-hepatanone, compounds that can inhibit NF-kappa B activation, partially prevented the TNF-alpha-induced decrease in myo-inositol accumulation. The effect of TNF-alpha on myo-inositol accumulation was also partially prevented by the protein kinase C inhibitor calphostin C but not by staurosporine. These studies demonstrate that TNF-alpha causes a decrease in SMIT mRNA levels and myo-inositol accumulation in cultured endothelial cells, which may be related to the activation of NF-kappa B.
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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/Carrier Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Growth Substances,
http://linkedlifedata.com/resource/pubmed/chemical/Heat-Shock Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Inositol,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/N-acetylsphingosine,
http://linkedlifedata.com/resource/pubmed/chemical/SLC5A3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Sphingosine,
http://linkedlifedata.com/resource/pubmed/chemical/Symporters,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
274
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
C58-71
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:9458713-Animals,
pubmed-meshheading:9458713-Aorta,
pubmed-meshheading:9458713-Carrier Proteins,
pubmed-meshheading:9458713-Cattle,
pubmed-meshheading:9458713-Cells, Cultured,
pubmed-meshheading:9458713-Cerebrovascular Circulation,
pubmed-meshheading:9458713-Cytokines,
pubmed-meshheading:9458713-Endothelium, Vascular,
pubmed-meshheading:9458713-Growth Substances,
pubmed-meshheading:9458713-Heat-Shock Proteins,
pubmed-meshheading:9458713-Humans,
pubmed-meshheading:9458713-Inositol,
pubmed-meshheading:9458713-Kinetics,
pubmed-meshheading:9458713-Membrane Proteins,
pubmed-meshheading:9458713-Mice,
pubmed-meshheading:9458713-Microcirculation,
pubmed-meshheading:9458713-Pulmonary Artery,
pubmed-meshheading:9458713-Sphingosine,
pubmed-meshheading:9458713-Symporters,
pubmed-meshheading:9458713-Transcription, Genetic,
pubmed-meshheading:9458713-Tumor Cells, Cultured,
pubmed-meshheading:9458713-Tumor Necrosis Factor-alpha
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pubmed:year |
1998
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pubmed:articleTitle |
Effect of TNF-alpha on SMIT mRNA levels and myo-inositol accumulation in cultured endothelial cells.
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pubmed:affiliation |
Department of Internal Medicine, University of Iowa, Iowa City 52246, USA.
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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.
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