Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1 Pt 1
pubmed:dateCreated
1998-2-19
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
274
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
C58-71
pubmed:dateRevised
2007-11-14
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
pubmed:year
1998
pubmed:articleTitle
Effect of TNF-alpha on SMIT mRNA levels and myo-inositol accumulation in cultured endothelial cells.
pubmed:affiliation
Department of Internal Medicine, University of Iowa, Iowa City 52246, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.