Linked Life Data

17629454

Source:http://linkedlifedata.com/resource/pubmed/id/17629454

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2007-7-27
pubmed:abstractText
We have recently demonstrated that endothelial beta(2) adrenergic receptors (beta(2)AR) regulate eNOS activity and consequently vascular tone, through means of PKB/AKT. In this work we explored the signal transduction pathway leading to AKT/eNOS activation in endothelial cells (EC). Using pharmacological and molecular inhibitors both in cultured EC cells and in ex vivo rat carotid preparations, we found that G(i) coupling of the beta(2)AR is needed for AKT activation and vasorelaxation. Since endothelial activation is sensitive to pertussis toxin but not to G(ibetagamma) inhibition by betaARKct, we conclude that G(alphai) mediates betaAR induced AKT activation. Downstream, betaAR signalling requires the soluble tyrosine kinase SRC, as both in cultured EC and rat carotid, the mutant dominant negative of SRC prevent beta(2)AR induced endothelial activation and vasodilation. In EC, G(alphai) directly interacts with SRC and this interaction leads to SRC activation and phosphorylation in a manner that is regulated by beta(2)AR stimulation. We propose a novel signal transduction pathway for beta(2)AR stimulation trough G(alphai) and SRC, leading to activation of AKT.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0898-6568
pubmed:author
pubmed:issnType
Print
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1949-55
pubmed:dateRevised
2011-9-22
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Endothelial beta2 adrenergic signaling to AKT: role of Gi and SRC.
pubmed:affiliation
Department of Clinical Medicine, Cardiovascular and Immunological Sciences, Federico II University, Naples, Italy.
pubmed:publicationType
Journal Article, In Vitro