Linked Life Data

20668227

Source:http://linkedlifedata.com/resource/pubmed/id/20668227

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
22
pubmed:dateCreated
2010-11-26
pubmed:abstractText
Endothelial cells (ECs) represent a major source of actively secreted adenosine triphosphate (ATP). Natural killer (NK) cells can mediate vascular injury in several pathologic conditions, including cytomegalovirus infection and vascular leak syndrome. We studied NK-cell expression of P2 receptors and the role of these nucleotide receptors in the regulation of endothelial-NK cell cross-talk. NK cells from healthy subjects expressed P2Y(?,?,?,?,??,??,??,??) and P2X(?,?,?,?,?) receptors. NK cells stimulated with ATP, but not uridine triphosphate, increased intracellular Ca²(+) and chemokinesis. Moreover, ATP, but not uridine triphosphate, inhibited NK chemotaxis in response to CX?CL1, whereas chemotaxis to CXCL12 was increased. CX?CL1 elicited killing of human umbilical vein ECs and human coronary artery ECs by NK cells. However, in the presence of ATP, CX?CL1 failed to stimulate killing of ECs. Such inhibitory effect was lost on exogenous addition of the ATP-hydrolyzing enzyme apyrase or by pharmacologic inhibition of the P2Y??R, and correlated with increased intracellular cyclic adenosine monophosphate concentrations induced by ATP or other P2Y??R agonists, including NAD(+). Extracellular ATP regulates NK-cell cytotoxicity via P2Y??R activation, protecting ECs from CX?CL1-elicited NK cell-mediated killing. These findings point out the P2Y??R as a potential target for pharmacologic intervention aimed at reducing NK-mediated vascular injury.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1528-0020
pubmed:author
pubmed:issnType
Electronic
pubmed:day
25
pubmed:volume
116
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4492-500
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
ATP secreted by endothelial cells blocks CX?CL 1-elicited natural killer cell chemotaxis and cytotoxicity via P2Y?? receptor activation.
pubmed:affiliation
Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), San Raffaele Pisana, Rome, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't