Coordinated Endothelial Nitric Oxide Synthase Activation by Translocation and Phosphorylation Determines Flow-Induced Nitric Oxide Production in Resistance Vessels

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dc.contributor.authorFigueroa, Xavier F.
dc.contributor.authorGonzalez, Daniel R.
dc.contributor.authorPuebla, Mariela
dc.contributor.authorAcevedo, Juan P.
dc.contributor.authorRojas-Libano, Daniel
dc.contributor.authorDuran, Walter N.
dc.contributor.authorBoric, Mauricio P.
dc.date.accessioned2025-01-24T00:07:28Z
dc.date.available2025-01-24T00:07:28Z
dc.date.issued2013
dc.description.abstractBackground/Aims: Endothelial nitric oxide synthase (eNOS) is associated with caveolin-1 (Cav-1) in plasma membrane. We tested the hypothesis that eNOS activation by shear stress in resistance vessels depends on synchronized phosphorylation, dissociation from Cav-1 and translocation of the membrane-bound enzyme to Golgi and cytosol. Methods: In isolated, perfused rat arterial mesenteric beds, we evaluated the effect of changes in flow rate (2-10 ml/min) on nitric oxide (NO) production, eNOS phosphorylation at serine 1177, eNOS subcellular distribution and co-immunoprecipitation with Cav-1, in the presence or absence of extracellular Ca2+. Results: Increases in flow induced a biphasic rise in NO production: a rapid transient phase (3-5-min) that peaked during the first 15 s, followed by a sustained phase, which lasted until the end of stimulation. Concomitantly, flow caused a rapid translocation of eNOS from the microsomal compartment to the cytosol and Golgi, paralleled by an increase in eNOS phosphorylation and a reduction in eNOS-Cav-1 association. Transient NO production, eNOS translocation and dissociation from Cav-1 depended on extracellular Ca2+, while sustained NO production was abolished by the PI3K-Akt blocker wortmannin. Conclusions: In intact resistance vessels, changes in flow induce NO production by transient Ca2+-dependent eNOS translocation from membrane to intracellular compartments and sustained Ca2+-independent PI3K-Akt-mediated phosphorylation. (C) 2013 S. Karger AG, Basel
dc.fuente.origenWOS
dc.identifier.doi10.1159/000355301
dc.identifier.eissn1423-0135
dc.identifier.issn1018-1172
dc.identifier.urihttps://doi.org/10.1159/000355301
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/101916
dc.identifier.wosidWOS:000327771600006
dc.issue.numero6
dc.language.isoen
dc.pagina.final511
dc.pagina.inicio498
dc.revistaJournal of vascular research
dc.rightsacceso restringido
dc.subjectEndothelial cells
dc.subjectResistance vessels
dc.subjectCa2+
dc.subjectShear stress
dc.subjectEndothelial nitric oxide synthase subcellular location
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleCoordinated Endothelial Nitric Oxide Synthase Activation by Translocation and Phosphorylation Determines Flow-Induced Nitric Oxide Production in Resistance Vessels
dc.typeartículo
dc.volumen50
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
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