Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3 Pt 1
pubmed:dateCreated
1997-4-24
pubmed:abstractText
Sphingosine derivatives are potent mitogens in several cell types. Many mitogens activate the Na+/H+ exchange, although the interrelationships between Na+/H+ exchange and mitogenesis are unclear. The present investigation in thyroid FRTL-5 cells shows that sphingosine 1-phosphate (SPP) activates Na+/H+ exchange in a dose-dependent manner in acid-loaded cells. The effect of SPP was abolished in a Na+-free buffer and by pretreatment of the cells with ethylisopropylamiloride. SPP did not affect basal intracellular pH (pHi). SPP stimulated the release of sequestered Ca2+ and a substantial entry of Ca2+. The effect of SPP on pH(i) was abolished in cells incubated in a Ca2+-free buffer, and in cells loaded with the intracellular Ca2+ chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid. Furthermore, the effect of SPP was abolished in pertussis toxin (PTX)-treated cells. PTX decreased Ca2+ entry only, without affecting the release from intracellular stores. Phosphatidic acid (PA) did not activate Na+/H+ exchange, suggesting that the effect of SPP was not mediated via activation of phospholipase D and the production of PA. Thus one mechanism of action of SPP in FRTL-5 cells appears to be to activate Na+/H+ exchange. This action is mediated via a G protein-dependent mechanism and requires an increase in intracellular free Ca2+.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
272
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
C1052-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Sphingosine 1-phosphate stimulates Na+/H+ exchange in thyroid FRTL-5 cells.
pubmed:affiliation
Department of Biosciences, University of Helsinki, Finland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't