2015
Endothelial Glucocorticoid Receptor Suppresses Atherogenesis—Brief Report
Goodwin JE, Zhang X, Rotllan N, Feng Y, Zhou H, Fernández-Hernando C, Yu J, Sessa WC. Endothelial Glucocorticoid Receptor Suppresses Atherogenesis—Brief Report. Arteriosclerosis Thrombosis And Vascular Biology 2015, 35: 779-782. PMID: 25810297, PMCID: PMC4375730, DOI: 10.1161/atvbaha.114.304525.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAortaAortic DiseasesApolipoproteins EAtherosclerosisBody WeightBrachiocephalic TrunkCholesterolDiet, High-FatDisease Models, AnimalEndothelial CellsGenotypeMacrophagesMice, Inbred C57BLMice, KnockoutPhenotypeReceptors, GlucocorticoidSeverity of Illness IndexTime FactorsTriglyceridesConceptsEndothelial glucocorticoid receptorGlucocorticoid receptorHigh-fat diet feedingApoE knockout backgroundSevere atherosclerotic lesionsGroups of micePathogenesis of atherosclerosisAortic sinusTotal cholesterolAtherosclerosis progressionBrachiocephalic arteryControl miceInflammatory milieuTonic inhibitionDiet feedingMacrophage recruitmentAtherosclerotic lesionsBody weightMiceKnockout backgroundReceptorsLesionsAtherosclerosisInflammationArtery
2010
Telmisartan regresses left ventricular hypertrophy in caveolin-1-deficient mice
Kreiger M, Di Lorenzo A, Teutsch C, Kauser K, Sessa WC. Telmisartan regresses left ventricular hypertrophy in caveolin-1-deficient mice. Laboratory Investigation 2010, 90: 1573-1581. PMID: 20585312, PMCID: PMC3248785, DOI: 10.1038/labinvest.2010.116.Peer-Reviewed Original ResearchConceptsCav-1 KO miceAngiotensin receptor blockersKO miceCardiac functionLV hypertrophyWT miceCardiac hypertrophyΒ-myosin heavy chainBody weight ratioTibial length ratioNatriuretic peptide ACaveolin-1-deficient miceCav-1 KOReceptor blockersPerivascular fibrosisVentricular hypertrophyVentricular weightAngiotensin IIIntramyocardial vesselsSpontaneous modelUnique genetic modelHypertrophyMiceTreatmentCaveolin-1
2000
In vivo delivery of the caveolin-1 scaffolding domain inhibits nitric oxide synthesis and reduces inflammation
Bucci M, Gratton J, Rudic R, Acevedo L, Roviezzo F, Cirino G, Sessa W. In vivo delivery of the caveolin-1 scaffolding domain inhibits nitric oxide synthesis and reduces inflammation. Nature Medicine 2000, 6: 1362-1367. PMID: 11100121, DOI: 10.1038/82176.Peer-Reviewed Original ResearchConceptsCaveolin-1Signal transductionSmall-molecule mimicryCaveolae assemblyInternalization sequenceCoat proteinEndothelial cellsPhysiological importanceEndothelial nitric oxide synthase (eNOS) inhibitorTransductionCholesterol transportNitric oxide synthase inhibitorChimeric peptideInhibits nitric oxide synthesisOxide synthase inhibitorNitric oxide synthesisNew therapeutic approachesNitric oxide productionSelective inhibitionDomainPeptidesCaveolinAcute inflammationCellsSystemic administrationAcute modulation of endothelial Akt/PKB activity alters nitric oxide–dependent vasomotor activity in vivo
Luo Z, Fujio Y, Kureishi Y, Rudic R, Daumerie G, Fulton D, Sessa W, Walsh K. Acute modulation of endothelial Akt/PKB activity alters nitric oxide–dependent vasomotor activity in vivo. Journal Of Clinical Investigation 2000, 106: 493-499. PMID: 10953024, PMCID: PMC380252, DOI: 10.1172/jci9419.Peer-Reviewed Original ResearchConceptsDN-AktEndothelial cell nitric oxide synthaseMyr-AktSerine/threonine protein kinase AktProtein kinase AktDominant-negative AktNitric oxideVasomotor toneFemoral arteryAkt functionReplication-defective adenoviral constructKinase AktActive AktEndothelium-dependent vasodilatationKey regulatorEndothelium-independent vasodilatorEndothelium-dependent vasomotionRabbit femoral artery modelNitric oxide synthaseAorta ex vivoImportant regulatorGene transferDoppler flow measurementsAktENOS inhibitorTemporal Events Underlying Arterial Remodeling After Chronic Flow Reduction in Mice
Rudic R, Bucci M, Fulton D, Segal S, Sessa W. Temporal Events Underlying Arterial Remodeling After Chronic Flow Reduction in Mice. Circulation Research 2000, 86: 1160-1166. PMID: 10850968, DOI: 10.1161/01.res.86.11.1160.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCarotid Artery, CommonCell DeathDrug CombinationsIn Vitro TechniquesMaleMiceMice, Inbred C57BLMuscle, Smooth, VascularNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIRegional Blood FlowTime FactorsTunica MediaVasodilator AgentsVasomotor SystemConceptsLeft common carotid arteryRight common carotid arteryCommon carotid arteryCarotid arteryBlood flowLeft external carotid arteryEndothelial NO synthase (eNOS) functionEndothelial NO synthase (eNOS) mRNAExternal carotid arteryNO synthase mRNANitrovasodilator sodium nitroprussideAcute ligationEndothelial dysfunctionArterial remodelingControl arteriesVascular remodelingAdult miceSodium nitroprussideDay 7Structural remodelingArteryLuminal remodelingMarked reductionProtein levelsMiceVasomotor control in arterioles of the mouse cremaster muscle
HUNGERFORD J, SESSA W, SEGAL S. Vasomotor control in arterioles of the mouse cremaster muscle. The FASEB Journal 2000, 14: 197-207. PMID: 10627294, DOI: 10.1096/fasebj.14.1.197.Peer-Reviewed Original ResearchConceptsMouse cremaster muscleVasomotor controlCremaster musclePerivascular sympathetic nerve stimulationAnesthetized C57Bl6 miceMicroiontophoresis of acetylcholineSympathetic nerve stimulationNitro-L-arginineConcentration-dependent vasoconstrictionBlood flow controlCremaster muscle preparationFocal vasoconstrictionVasodilatory responseNerve stimulationTransgenic mouse technologyVasomotor responsesC57BL6 miceCardiovascular functionNormal miceMuscle preparationsArteriolesBiphasic responseIntravital microscopyAcetylcholineVasoconstriction
1996
Elevated blood pressures in mice lacking endothelial nitric oxide synthase
Shesely E, Maeda N, Kim H, Desai K, Krege J, Laubach V, Sherman P, Sessa W, Smithies O. Elevated blood pressures in mice lacking endothelial nitric oxide synthase. Proceedings Of The National Academy Of Sciences Of The United States Of America 1996, 93: 13176-13181. PMID: 8917564, PMCID: PMC24066, DOI: 10.1073/pnas.93.23.13176.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAnimalsBlood PressureCattleChimeraDNA PrimersEndothelium, VascularFemaleGenotypeHeterozygoteHypertensionIsoenzymesKidneyLipopolysaccharidesMaleMiceMice, Inbred C57BLMice, KnockoutNitric Oxide SynthasePolymerase Chain ReactionReninRNA, MessengerStem CellsTranscription, GeneticConceptsEndothelial nitric oxide synthaseBlood pressureNitric oxide synthaseHeart rateENOS proteinOxide synthaseENOS mutant miceLipopolysaccharide-induced deathElevated blood pressureNormal blood pressurePlasma renin concentrationBlood pressure regulationLower body weightKidney renin mRNAAnti-eNOS antibodiesAppropriate genetic controlsENOS locusENOS genotypesRenin concentrationVascular toneFemale miceRenin mRNAENOS geneENOS mutationBody weight