2021
Alcohol-induced Hsp90 acetylation is a novel driver of liver sinusoidal endothelial dysfunction and alcohol-related liver disease
Yang Y, Sangwung P, Kondo R, Jung Y, McConnell MJ, Jeong J, Utsumi T, Sessa WC, Iwakiri Y. Alcohol-induced Hsp90 acetylation is a novel driver of liver sinusoidal endothelial dysfunction and alcohol-related liver disease. Journal Of Hepatology 2021, 75: 377-386. PMID: 33675874, PMCID: PMC8292196, DOI: 10.1016/j.jhep.2021.02.028.Peer-Reviewed Original ResearchConceptsEndothelial nitric oxide synthaseAlcohol-induced liver injuryLiver sinusoidal endothelial cellsAlcohol-related liver diseaseLiver injuryLSEC dysfunctionHsp90 acetylationNO productionHistone deacetylase 6Liver diseaseTherapeutic strategiesHeat shock protein 90 (Hsp90) acetylationLiver sinusoidal endothelial dysfunctionSinusoidal endothelial cell dysfunctionMouse liver sinusoidal endothelial cellsEndothelial cell dysfunctionNitric oxide synthaseEthanol-fed miceSinusoidal endothelial dysfunctionPotential therapeutic approachPotential therapeutic strategyNitric oxide productionNew therapeutic strategiesSinusoidal endothelial cellsAcetylation of Hsp90
2019
Caveolin-1 Regulates Atherogenesis by Attenuating Low-Density Lipoprotein Transcytosis and Vascular Inflammation Independently of Endothelial Nitric Oxide Synthase Activation
Ramírez CM, Zhang X, Bandyopadhyay C, Rotllan N, Sugiyama MG, Aryal B, Liu X, He S, Kraehling JR, Ulrich V, Lin CS, Velazquez H, Lasunción MA, Li G, Suárez Y, Tellides G, Swirski FK, Lee WL, Schwartz MA, Sessa WC, Fernández-Hernando C. Caveolin-1 Regulates Atherogenesis by Attenuating Low-Density Lipoprotein Transcytosis and Vascular Inflammation Independently of Endothelial Nitric Oxide Synthase Activation. Circulation 2019, 140: 225-239. PMID: 31154825, PMCID: PMC6778687, DOI: 10.1161/circulationaha.118.038571.Peer-Reviewed Original ResearchConceptsEndothelial nitric oxide synthaseDiet-induced atherosclerosisNO productionVascular inflammationENOS activationEndothelial nitric oxide synthase activationNitric oxide synthase activationAthero-protective functionsLipid metabolic factorsEndothelial cell inflammationNitric oxide synthaseWild-type miceMice Lacking ExpressionProduction of NOExtracellular matrix remodelingInflammatory primingHyperlipidemic miceInflammatory pathwaysAortic archCell inflammationOxide synthaseMetabolic factorsMouse modelAtherosclerosisInflammationAndrogens drive microvascular endothelial dysfunction in women with polycystic ovary syndrome: role of the endothelin B receptor
Usselman CW, Yarovinsky T, Steele FE, Leone CA, Taylor HS, Bender JR, Stachenfeld NS. Androgens drive microvascular endothelial dysfunction in women with polycystic ovary syndrome: role of the endothelin B receptor. The Journal Of Physiology 2019, 597: 2853-2865. PMID: 30847930, DOI: 10.1113/jp277756.Peer-Reviewed Original ResearchMeSH KeywordsAdultAndrogensCardiovascular DiseasesDihydrotestosteroneEndothelin-1Endothelium, VascularEstrogensEthinyl EstradiolFemaleGlucose Tolerance TestHumansMicrovesselsNitric OxideObesityPolycystic Ovary SyndromeReceptor, Endothelin BSkinVascular Endothelial Growth Factor AVasodilationYoung AdultConceptsPolycystic ovary syndromeCardiovascular dysfunctionEndothelial dysfunctionOvary syndromeEndothelin-1Endothelial functionNO productionAndrogen receptor-dependent mannerEndothelin-B receptor subtypeCardiovascular risk factorsMicrovascular endothelial dysfunctionMicrovascular endothelial functionCutaneous vascular conductanceB receptor subtypesEndothelin B receptorLaser Doppler flowmetryNitric oxide inhibitionReceptor-dependent mannerEndothelial cell NO productionDose-response curveVasodilating responsePCOS subjectsLean womenObese womenVascular conductance
2016
AMP‐Activated Protein Kinase Attenuates High Salt‐Induced Activation of Epithelial Sodium Channels (ENaC) in Human Umbilical Vein Endothelial Cells
Zheng W, Li X, Liu H, Wang Z, Hu Q, Li Y, Song B, Lou J, Wang Q, Ma H, Zhang Z. AMP‐Activated Protein Kinase Attenuates High Salt‐Induced Activation of Epithelial Sodium Channels (ENaC) in Human Umbilical Vein Endothelial Cells. Oxidative Medicine And Cellular Longevity 2016, 2016: 1531392. PMID: 27635187, PMCID: PMC5011216, DOI: 10.1155/2016/1531392.Peer-Reviewed Original ResearchConceptsAMP-activated kinaseAMP-activated kinase activityHuman umbilical vein endothelial cellsEpithelial sodium channelAMP-activated protein kinaseUmbilical vein endothelial cellsEndothelial cellsVein endothelial cellsActivity of epithelial sodium channelsCell-attached patch-clamp techniqueSodium channelsNO productionHigh-sodiumENOS phosphorylationProtein kinaseENaC open probabilityEffects of high sodiumPatch-clamp techniqueSodium treatmentPhosphorylationHigh saltNitric oxide synthaseExpression levelsENaC blockersENaC expression
2014
Selective Serotonin Reuptake Inhibitors and Endothelial Function in Women
Hantsoo L, Czarkowski KA, Child J, Howes C, Epperson CN. Selective Serotonin Reuptake Inhibitors and Endothelial Function in Women. Journal Of Women's Health 2014, 23: 613-618. PMID: 24886268, PMCID: PMC4089019, DOI: 10.1089/jwh.2013.4623.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultBlood Flow VelocityBrachial ArteryDepression, PostpartumDepressive Disorder, MajorEndothelium, VascularFemaleFollow-Up StudiesHumansMiddle AgedNitric OxidePlatelet AggregationPremenstrual SyndromeSelective Serotonin Reuptake InhibitorsTreatment OutcomeUltrasonography, DopplerVasodilationYoung AdultConceptsSelective serotonin reuptake inhibitorsSerotonin reuptake inhibitorsSSRI treatmentPremenstrual dysphoric disorderCardiovascular diseasePlatelet aggregationNO productionReuptake inhibitorsPostpartum depressionEffects of SSRIsBurden of diseasePlatelet NO productionDepression/anxietyNitric oxide functionSSRI therapyEndothelial functionVascular mechanismsVascular dilatationMajor depressionDysphoric disorderNormal rangeBeck DepressionYounger groupDiseaseWomen
2012
Plac8-Dependent and Inducible NO Synthase-Dependent Mechanisms Clear Chlamydia muridarum Infections from the Genital Tract
Johnson RM, Kerr MS, Slaven JE. Plac8-Dependent and Inducible NO Synthase-Dependent Mechanisms Clear Chlamydia muridarum Infections from the Genital Tract. The Journal Of Immunology 2012, 188: 1896-1904. PMID: 22238459, PMCID: PMC3303601, DOI: 10.4049/jimmunol.1102764.Peer-Reviewed Original ResearchConceptsGenital tract infectionCD4 T-cell clonesINOS-independent mechanismCD4 T cellsT cell clonesTract infectionsT cellsC. muridarum genital tract infectionCell clonesChlamydia muridarum infectionInducible NO synthase (iNOS) transcriptionT cell mechanismsT cell subsetsClearance of infectionGenital tract epitheliumT cell degranulationCytokine profileCell subsetsCell degranulationGenital tractClear infectionEffector functionsMouse modelNO productionVaccine development
2011
A Metronidazole-Resistant Isolate of Blastocystis spp. Is Susceptible to Nitric Oxide and Downregulates Intestinal Epithelial Inducible Nitric Oxide Synthase by a Novel Parasite Survival Mechanism
Mirza H, Wu Z, Kidwai F, Tan KS. A Metronidazole-Resistant Isolate of Blastocystis spp. Is Susceptible to Nitric Oxide and Downregulates Intestinal Epithelial Inducible Nitric Oxide Synthase by a Novel Parasite Survival Mechanism. Infection And Immunity 2011, 79: 5019-5026. PMID: 21930763, PMCID: PMC3232666, DOI: 10.1128/iai.05632-11.Peer-Reviewed Original ResearchConceptsInducible nitric oxide synthaseMetronidazole-resistant isolatesNitric oxide synthaseNitric oxideOxide synthaseBlastocystis infectionEpithelial inducible nitric oxide synthaseST-7Dose-dependent inhibitionHost innate responseHuman intestinal epitheliumHost defense mechanismsIntestinal epithelial cellsLuminal pathogensAbdominal painIntestinal symptomsImmunocompetent patientsST-4Caco-2 modelChronic infectionControversial pathogenesisInnate responseNO productionBlastocystis sppIntestinal epithelium
2010
“Arginine paradox” in cardiomyocytes of Sprague Dawley and spontaneously hypertensive rats: α2-adrenoreceptor-mediated regulation of L-type Ca2+ currents by L-arginine
Nenov M, Berezhnov A, Fedotova E, Grushin K, Pimenov O, Murashev A, Zinchenko V, Kokoz Y. “Arginine paradox” in cardiomyocytes of Sprague Dawley and spontaneously hypertensive rats: α2-adrenoreceptor-mediated regulation of L-type Ca2+ currents by L-arginine. Biochemistry (Moscow), Supplement Series A: Membrane And Cell Biology 2010, 4: 374-382. DOI: 10.1134/s1990747810040070.Peer-Reviewed Original ResearchChlamydia-Specific CD4 T Cell Clones Control Chlamydia muridarum Replication in Epithelial Cells by Nitric Oxide-Dependent and -Independent Mechanisms
Jayarapu K, Kerr M, Ofner S, Johnson RM. Chlamydia-Specific CD4 T Cell Clones Control Chlamydia muridarum Replication in Epithelial Cells by Nitric Oxide-Dependent and -Independent Mechanisms. The Journal Of Immunology 2010, 185: 6911-6920. PMID: 21037093, PMCID: PMC3073083, DOI: 10.4049/jimmunol.1002596.Peer-Reviewed Original ResearchConceptsCD4 T-cell clonesT cell clonesEpithelial NO productionCD4 T cellsChlamydia replicationCell clonesEpithelial cellsT cellsNO productionReproductive tract epithelial cellsT cell-mediated controlT-cell depletion studiesCell depletion studiesCell-mediated controlHuman reproductive tractT cell degranulationMHC class IIMurine genital tractTract epithelial cellsInfected epithelial cellsEpithelial tumor cell linesIntracellular bacterial pathogenBacterial clearanceCell degranulationGenital tract
2004
17β-Estradiol Exposure Leads to Activation of ERK and p38 but Not JNK in Vascular Endothelial Cells
Knox R, Chen E, Wang X, Jeffries B, Yamaguchi M, Kim S, Sumpio B. 17β-Estradiol Exposure Leads to Activation of ERK and p38 but Not JNK in Vascular Endothelial Cells. International Journal Of Angiology 2004, 13: 67-70. DOI: 10.1007/s00547-004-1068-9.Peer-Reviewed Original ResearchEndothelial nitric oxide synthaseVascular endothelial cellsBovine aortic endothelial cellsEndothelial cellsNitric oxideNitric oxide synthaseEndothelial NO productionAnti-phosphospecific antibodiesEndothelial cell productionAortic endothelial cellsRapid activationAtheroprotective effectsActivation of ERKOxide synthaseFetal calf serumE2 exposureNO productionENOS activationActivity of JNKEstrogenBiphasic patternP38 phosphorylationMonophasic mannerTotal ERKERK phosphorylationHistamine inhibits conducted vasodilation through endothelium‐derived NO production in arterioles of mouse skeletal muscle
Payne GW, Madri JA, Sessa WC, Segal SS. Histamine inhibits conducted vasodilation through endothelium‐derived NO production in arterioles of mouse skeletal muscle. The FASEB Journal 2004, 18: 280-286. PMID: 14769822, DOI: 10.1096/fj.03-0752com.Peer-Reviewed Original ResearchMeSH KeywordsAcetylcholineAnimalsArteriolesEndothelium, VascularFemaleGene DeletionGuanylate CyclaseHistamineMaleMiceMice, Inbred C57BLMice, KnockoutMuscle, SkeletalNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIPlatelet Endothelial Cell Adhesion Molecule-1VasodilationConceptsENOS-/- miceArteriolar endotheliumEndothelium-derived NO productionSpread of hyperpolarizationNO-dependent mechanismSecond-order arteriolesIntercellular adhesion moleculeGap junction channelsSoluble guanylate cyclaseAcetylcholine microiontophoresisHistamine inhibitsLocal vasodilationMouse skeletal muscleNO synthaseVenular endotheliumVasodilationCremaster muscleMaximal diameterNO productionArteriolesHistamineJunction channelsGuanylate cyclaseEndotheliumAdhesion molecules17β-Estradiol exposure leads to activation of ERK and p38 but not JNK in vascular endothelial cells
Knox R, Chen E, Wang X, Jeffries B, Yamaguchi M, Kim S, Sumpio B. 17β-Estradiol exposure leads to activation of ERK and p38 but not JNK in vascular endothelial cells. International Journal Of Angiology 2004, 67-70. DOI: 10.1055/s-0031-1276450.Peer-Reviewed Original ResearchEndothelial nitric oxide synthaseVascular endothelial cellsBovine aortic endothelial cellsEndothelial cellsNitric oxideNitric oxide synthaseEndothelial NO productionAnti-phosphospecific antibodiesEndothelial cell productionAortic endothelial cellsRapid activationAtheroprotective effectsActivation of ERKOxide synthaseFetal calf serumE2 exposureNO productionENOS activationActivity of JNKEstrogenBiphasic patternP38 phosphorylationMonophasic mannerTotal ERKERK phosphorylation
2003
Bacterial translocation up‐regulates GTP‐cyclohydrolase I in mesenteric vasculature of cirrhotic rats
Wiest R, Cadelina G, Milstien S, McCuskey RS, Garcia‐Tsao G, Groszmann RJ. Bacterial translocation up‐regulates GTP‐cyclohydrolase I in mesenteric vasculature of cirrhotic rats. Hepatology 2003, 38: 1508-1515. PMID: 14647062, DOI: 10.1016/j.hep.2003.09.039.Peer-Reviewed Original ResearchConceptsBacterial translocationMesenteric lymph nodesMesenteric vasculatureGTPCH I activitySerum endotoxinCirrhotic ratsNitric oxideSerum NOx levelsVascular NO productionStandard bacteriologic cultureEssential cofactor tetrahydrobiopterinLimulus amebocyte lysate assayArterial vasodilationArterial pressureLymph nodesHemodynamic disturbancesMesenteric circulationSystemic appearanceEndotoxemiaNO productionBacteriologic cultureNOx levelsCofactor tetrahydrobiopterinEndotoxinLysate assay
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
2000
Simvastatin upregulates coronary vascular endothelial nitric oxide production in conscious dogs
Mital S, Zhang X, Zhao G, Bernstein R, Smith C, Fulton D, Sessa W, Liao J, Hintze T. Simvastatin upregulates coronary vascular endothelial nitric oxide production in conscious dogs. AJP Heart And Circulatory Physiology 2000, 279: h2649-h2657. PMID: 11087217, DOI: 10.1152/ajpheart.2000.279.6.h2649.Peer-Reviewed Original ResearchMeSH KeywordsAcetylcholineAdenosineAnimalsAnticholesteremic AgentsConsciousnessCoronary CirculationDogsEndothelium, VascularEnzyme InhibitorsGene Expression Regulation, EnzymologicHeart RateIn Vitro TechniquesMicrocirculationMyocardiumNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type IIINitritesNitroglycerinOxygen ConsumptionRNA, MessengerSimvastatinVasodilationVasodilator AgentsVeratrineConceptsEndothelial nitric oxide synthaseCoronary blood flowCoronary vasodilationConscious dogsSimvastatin administrationVascular endothelial nitric oxide productionVascular endothelial nitric oxide synthaseNO productionEndothelial nitric oxide productionEndothelium-independent vasodilatorCoronary vascular endotheliumShort-term administrationLipid-lowering effectsNitric oxide synthaseEndothelial NO productionMyocardial oxygen consumptionNitric oxide productionNO-dependent regulationPlasma nitrateGeneral anesthesiaENOS proteinCoronary microvesselsOxide synthaseMongrel dogsENOS mRNA
1999
Hsp90 regulation of endothelial nitric oxide synthase contributes to vascular control in portal hypertension
Shah V, Wiest R, Garcia-Cardena G, Cadelina G, Groszmann R, Sessa W. Hsp90 regulation of endothelial nitric oxide synthase contributes to vascular control in portal hypertension. American Journal Of Physiology 1999, 277: g463-g468. PMID: 10444461, DOI: 10.1152/ajpgi.1999.277.2.g463.Peer-Reviewed Original ResearchMeSH KeywordsAcetylcholineAnimalsBenzoquinonesBlood VesselsHSP90 Heat-Shock ProteinsHypertension, PortalIn Vitro TechniquesLactams, MacrocyclicMaleMethoxamineMicrocirculationNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type IIIQuinonesRatsRats, Sprague-DawleySplanchnic CirculationTissue DistributionVasoconstrictor AgentsVasodilationVasodilator AgentsConceptsEndothelial nitric oxide synthasePortal vein ligationNitric oxide synthasePortal hypertensionMesenteric vasculatureOxide synthaseNormal animalsACh-dependent vasodilationExperimental portal hypertensionExcessive NO productionNO-dependent responsesNOS catalytic activityDependent vasodilationVein ligationVascular controlMesenteric circulationPVL animalsMesenteric vesselsHeat shock protein 90Sodium nitroprussideNO productionEndothelial liningHypertensionShock protein 90MethoxamineNitric oxide production and absorption in trachea, bronchi, bronchioles, and respiratory bronchioles of humans
DuBois A, Kelley P, Douglas J, Mohsenin V. Nitric oxide production and absorption in trachea, bronchi, bronchioles, and respiratory bronchioles of humans. Journal Of Applied Physiology 1999, 86: 159-167. PMID: 9887126, DOI: 10.1152/jappl.1999.86.1.159.Peer-Reviewed Original Research
1995
Native low-density lipoprotein increases endothelial cell nitric oxide synthase generation of superoxide anion.
Pritchard K, Groszek L, Smalley D, Sessa W, Wu M, Villalon P, Wolin M, Stemerman M. Native low-density lipoprotein increases endothelial cell nitric oxide synthase generation of superoxide anion. Circulation Research 1995, 77: 510-8. PMID: 7543827, DOI: 10.1161/01.res.77.3.510.Peer-Reviewed Original ResearchConceptsLow-density lipoproteinNative low-density lipoproteinN-LDLNitro-L-arginine methyl esterNitric oxideLevels of nitrotyrosineEndothelial cell releaseEC releaseThiobarbituric acid substancesFormation of peroxynitriteSuperoxide anionENOS activityL-arginineNO productionSKF-525ANitrite productionOxidative metabolismAn Inhibitor of Macrophage Arginine Transport and Nitric Oxide Production (CNI-1493) Prevents Acute Inflammation and Endotoxin Lethality
Bianchi M, Ulrich P, Bloom O, Meistrell M, Zimmerman G, Schmidtmayerova H, Bukrinsky M, Donnelley T, Bucala R, Sherry B, Manogue K, Tortolani A, Cerami A, Tracey K. An Inhibitor of Macrophage Arginine Transport and Nitric Oxide Production (CNI-1493) Prevents Acute Inflammation and Endotoxin Lethality. Molecular Medicine 1995, 1: 254-266. PMID: 8529104, PMCID: PMC2229913, DOI: 10.1007/bf03401550.Peer-Reviewed Original ResearchConceptsNitric oxide synthaseL-arginine transportNO productionInflammatory responseBlood vesselsEndotoxin lethalityEDRF activityL-arginineArginine transportInhibitor of NOSLethal LPS challengeSystemic inflammatory responseNitric oxide productionSelective inhibitorDevelopment of carrageenanProduction of NOBackgroundNitric oxideEDRF responseMurine macrophage-like cell lineTetravalent guanylhydrazoneFootpad inflammationImportant homeostatic mechanismAcute inflammationLPS challengeMacrophage-like cell line
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