Linked Life Data

15632208

Source:http://linkedlifedata.com/resource/pubmed/id/15632208

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2005-4-1
pubmed:abstractText
Sphingosine-1-phosphate (S1P), the bioactive product of sphingosine kinase (SK) activation, is a survival factor for endothelial cells. The mechanism of SK-mediated survival was investigated in endothelial cells with moderately raised intracellular SK activity. Overexpression of SK mediated survival primarily through the activation of the phosphatidyl inositol 3-kinase (PI-3K)/protein kinase B (Akt/PKB) pathway and an associated up-regulation of the antiapoptotic protein B cell lymphoma gene 2 (Bcl-2) and down-regulation of the proapoptotic protein bisindolylmaleimide (Bcl-2 interacting mediator of cell death; Bim). In addition there was an up-regulation and dephosphorylation of the junctional molecule platelet endothelial cell adhesion molecule-1 (PECAM-1), which was obligatory for activation of the PI-3K/Akt pathway, for SK-induced cell survival, and for the changes in the apoptosis-related proteins. Thus, raised intracellular SK activity induced a molecule involved in cell-cell interactions to augment cell survival through a PI-3K/Akt-dependent pathway. This is distinct from the activation of both PI-3K/Akt and mitogen-activated protein kinase (MAPK) pathways seen with exogenously added S1P. Cells overexpressing SK showed enhanced survival under conditions of serum deprivation and absence of attachment to extracellular matrix, suggesting a role for SK in the regulation of vascular phenomena that occur under conditions of stress, such as angiogenesis and survival in unattached states, as would be required for a circulating endothelial cell.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
105
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3169-77
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:15632208-Antigens, CD31, pubmed-meshheading:15632208-Apoptosis, pubmed-meshheading:15632208-Cell Survival, pubmed-meshheading:15632208-Cells, Cultured, pubmed-meshheading:15632208-Culture Media, Serum-Free, pubmed-meshheading:15632208-Endothelium, Vascular, pubmed-meshheading:15632208-Gene Expression Regulation, Enzymologic, pubmed-meshheading:15632208-Humans, pubmed-meshheading:15632208-Neovascularization, Physiologic, pubmed-meshheading:15632208-Phosphatidylinositol 3-Kinases, pubmed-meshheading:15632208-Phosphorylation, pubmed-meshheading:15632208-Phosphotransferases (Alcohol Group Acceptor), pubmed-meshheading:15632208-Protein-Serine-Threonine Kinases, pubmed-meshheading:15632208-Proto-Oncogene Proteins, pubmed-meshheading:15632208-Proto-Oncogene Proteins c-akt, pubmed-meshheading:15632208-Proto-Oncogene Proteins c-bcl-2, pubmed-meshheading:15632208-Signal Transduction, pubmed-meshheading:15632208-Umbilical Veins
pubmed:year
2005
pubmed:articleTitle
Sphingosine kinase-1 enhances endothelial cell survival through a PECAM-1-dependent activation of PI-3K/Akt and regulation of Bcl-2 family members.
pubmed:affiliation
Hanson Institute, Institute of Medical and Veterinary Science, Adelaide, SA, Australia.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't