2013
eNOS-derived nitric oxide regulates endothelial barrier function through VE-cadherin and Rho GTPases
Di Lorenzo A, Lin MI, Murata T, Landskroner-Eiger S, Schleicher M, Kothiya M, Iwakiri Y, Yu J, Huang PL, Sessa WC. eNOS-derived nitric oxide regulates endothelial barrier function through VE-cadherin and Rho GTPases. Journal Of Cell Science 2013, 126: 5541-5552. PMID: 24046447, PMCID: PMC3860306, DOI: 10.1242/jcs.115972.Peer-Reviewed Original ResearchMeSH KeywordsAdherens JunctionsAnimalsAntigens, CDCadherinsCapillary PermeabilityCells, CulturedCSK Tyrosine-Protein KinaseEndothelial CellsEndothelium, VascularGuanine Nucleotide Exchange FactorsHumansMaleMiceMice, Inbred C57BLMice, KnockoutNitric OxideNitric Oxide Synthase Type IIIPhosphorylationProtein Processing, Post-TranslationalProtein TransportSrc-Family KinasesStress FibersT-Lymphoma Invasion and Metastasis-inducing Protein 1Vascular Endothelial Growth Factor AConceptsAdherens junctionsVE-cadherinExchange factor Tiam1Vascular endothelial growth factorStress fiber formationEndothelial NO synthaseEndothelial adherens junctionsVE-cadherin phosphorylationCytoskeletal architectureRho GTPasesCortical actinCytoskeletal remodelingRac GTPaseC-SrcRac guanineRho activationMolecular mechanismsPhysiological roleEndothelial barrier functionFiber formationENOS activationGrowth factorEnhanced activationActivationNitric oxide
2004
Targeting of Endothelial Nitric-oxide Synthase to the Cytoplasmic Face of the Golgi Complex or Plasma Membrane Regulates Akt- Versus Calcium-dependent Mechanisms for Nitric Oxide Release*
Fulton D, Babbitt R, Zoellner S, Fontana J, Acevedo L, McCabe TJ, Iwakiri Y, Sessa WC. Targeting of Endothelial Nitric-oxide Synthase to the Cytoplasmic Face of the Golgi Complex or Plasma Membrane Regulates Akt- Versus Calcium-dependent Mechanisms for Nitric Oxide Release*. Journal Of Biological Chemistry 2004, 279: 30349-30357. PMID: 15136572, DOI: 10.1074/jbc.m402155200.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlotting, WesternCalciumCalmodulinCell MembraneCOS CellsCysteineCytoplasmEndothelium, VascularGolgi ApparatusHumansMicroscopy, FluorescenceMyristic AcidsNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type IIIPalmitic AcidsPhosphorylationProtein Serine-Threonine KinasesProtein Structure, TertiaryProto-Oncogene ProteinsProto-Oncogene Proteins c-aktSerineTransfectionUmbilical VeinsConceptsPlasma membraneGolgi complexAkt-dependent phosphorylationEndothelial nitricoxide synthasePool of enzymesCalcium-dependent activationCytoplasmic faceGolgi membranesENOS constructMembrane versionFusion proteinCytoplasmic aspectFunctional rolePhosphorylationENOS activationHeterogeneous localizationMembraneCalcium fluxCalcium-dependent mechanismSynthaseActivationEndothelial nitric oxide synthaseFurther activationComplexesNitricoxide synthase
2002
Phosphorylation of eNOS initiates excessive NO production in early phases of portal hypertension
Iwakiri Y, Tsai MH, McCabe TJ, Gratton JP, Fulton D, Groszmann RJ, Sessa WC. Phosphorylation of eNOS initiates excessive NO production in early phases of portal hypertension. AJP Heart And Circulatory Physiology 2002, 282: h2084-h2090. PMID: 12003815, DOI: 10.1152/ajpheart.00675.2001.Peer-Reviewed Original ResearchMeSH KeywordsAdrenergic alpha-1 Receptor AgonistsAndrostadienesAnimalsEnzyme InhibitorsHypertension, PortalLigationMaleMesenteric Artery, SuperiorMethoxamineNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type IIIOmega-N-MethylargininePhosphorylationPortal VeinProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleyVasoconstrictor AgentsWortmanninConceptsEndothelial nitric oxide synthasePortal vein ligationPhosphorylation of eNOSMesenteric arterial bedPortal hypertensionPVL groupArterial bedNO productionMale Sprague-Dawley ratsEarly portal hypertensionMonomethyl-L-arginineNitric oxide synthaseSprague-Dawley ratsExcessive NO productionG protein-coupled receptorsVivo perfusion studiesPVL ratsProtein-coupled receptorsPerfusion pressureSham groupVein ligationENOS expressionOxide synthaseReduced responsivenessKinase/Akt pathway