| http://purl.uniprot.org/citations/18952717 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/18952717 | http://www.w3.org/2000/01/rdf-schema#comment | "During an agonist stimulation of endothelial cells, the sustained Ca2+ entry occurring through store-operated channels has been shown to significantly contribute to smooth muscle relaxation through the release of relaxing factors such as nitric oxide (NO). However, the mechanisms linking Ca2+ stores depletion to the opening of such channels are still elusive. We have used Ca2+ and tension measurements in intact aortic strips to investigate the role of the Ca2+-independent isoform of phospholipase A2 (iPLA2) in endothelial store-operated Ca2+ entry and endothelium-dependent relaxation of smooth muscle. We provide evidence that iPLA2 is involved in the activation of endothelial store-operated Ca2+ entry when Ca2+ stores are artificially depleted. We also show that the sustained store-operated Ca2+ entry occurring during physiological stimulation of endothelial cells with the circulating hormone ATP is due to iPLA2 activation and significantly contributes to the amplitude and duration of ATP-induced endothelium-dependent relaxation. Consistently, both iPLA2 metabolites arachidonic acid and lysophosphatidylcholine were found to stimulate Ca2+ entry in native endothelial cells. However, only the latter triggered endothelium-dependent relaxation through NO release, suggesting that lysophosphatidylcholine produced by iPLA2 upon Ca2+ stores depletion may act as an intracellular messenger that stimulates store-operated Ca2+ entry and subsequent NO production in endothelial cells. Finally, we found that ACh-induced endothelium relaxation also depends on iPLA2 activation, suggesting that the iPLA2-dependent control of endothelial store-operated Ca2+ entry is a key physiological mechanism regulating arterial tone."xsd:string |
| http://purl.uniprot.org/citations/18952717 | http://purl.org/dc/terms/identifier | "doi:10.1152/ajpheart.00639.2008"xsd:string |
| http://purl.uniprot.org/citations/18952717 | http://purl.uniprot.org/core/author | "Beny J.L."xsd:string |
| http://purl.uniprot.org/citations/18952717 | http://purl.uniprot.org/core/author | "Boittin F.X."xsd:string |
| http://purl.uniprot.org/citations/18952717 | http://purl.uniprot.org/core/author | "Gribi F."xsd:string |
| http://purl.uniprot.org/citations/18952717 | http://purl.uniprot.org/core/author | "Serir K."xsd:string |
| http://purl.uniprot.org/citations/18952717 | http://purl.uniprot.org/core/date | "2008"xsd:gYear |
| http://purl.uniprot.org/citations/18952717 | http://purl.uniprot.org/core/name | "Am J Physiol Heart Circ Physiol"xsd:string |
| http://purl.uniprot.org/citations/18952717 | http://purl.uniprot.org/core/pages | "H2466-74"xsd:string |
| http://purl.uniprot.org/citations/18952717 | http://purl.uniprot.org/core/title | "Ca2+-independent PLA2 controls endothelial store-operated Ca2+ entry and vascular tone in intact aorta."xsd:string |
| http://purl.uniprot.org/citations/18952717 | http://purl.uniprot.org/core/volume | "295"xsd:string |
| http://purl.uniprot.org/citations/18952717 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/18952717 |
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