2015
Diverse contribution of bone marrow-derived late-outgrowth endothelial progenitor cells to vascular repair under pulmonary arterial hypertension and arterial neointimal formation
Ikutomi M, Sahara M, Nakajima T, Minami Y, Morita T, Hirata Y, Komuro I, Nakamura F, Sata M. Diverse contribution of bone marrow-derived late-outgrowth endothelial progenitor cells to vascular repair under pulmonary arterial hypertension and arterial neointimal formation. Journal Of Molecular And Cellular Cardiology 2015, 86: 121-135. PMID: 26231083, DOI: 10.1016/j.yjmcc.2015.07.019.Peer-Reviewed Original ResearchConceptsPulmonary arterial hypertensionEndothelial progenitor cellsLate outgrowth endothelial progenitor cellsEarly endothelial progenitor cellsFemoral arteryVascular repairEPC subpopulationsArterial hypertensionArterial neointimal formationProgenitor cellsBM mononuclear cellsNeointimal lesion formationFisher 344 ratsEPC treatmentEnhanced proliferation potentialPulmonary arteriolesPulmonary arteryPulmonary vasculatureEndovascular injuryMononuclear cellsVascular diseaseSystemic arteriesTherapeutic effectNeointimal formationInflammatory genes
2012
Nicorandil Attenuates Monocrotaline-Induced Vascular Endothelial Damage and Pulmonary Arterial Hypertension
Sahara M, Sata M, Morita T, Hirata Y, Nagai R. Nicorandil Attenuates Monocrotaline-Induced Vascular Endothelial Damage and Pulmonary Arterial Hypertension. PLOS ONE 2012, 7: e33367. PMID: 22479390, PMCID: PMC3316574, DOI: 10.1371/journal.pone.0033367.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntihypertensive AgentsApoptosisBlotting, WesternCaspase 3Cells, CulturedDrug Therapy, CombinationEndothelium, VascularEnzyme InhibitorsFamilial Primary Pulmonary HypertensionGlyburideHuman Umbilical Vein Endothelial CellsHumansHypertension, PulmonaryInjections, IntraperitonealMaleMAP Kinase Signaling SystemMonocrotalineNG-Nitroarginine Methyl EsterNicorandilPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRandom AllocationRatsRats, Sprague-DawleySignal TransductionVentricular PressureConceptsRight ventricular systolic pressurePulmonary arterial hypertensionHuman umbilical vein endothelial cellsVascular endothelial damageMCT injectionArterial hypertensionEndothelial damageNitro-L-arginine methyl esterNitric oxide synthase inhibitorBeneficial effectsEndothelial NOS expressionVentricular systolic pressureVehicle-treated groupChannel blocker glibenclamideOxide synthase inhibitorChannel opener nicorandilSprague-Dawley ratsCaspase-3 expressionAnti-apoptotic effectsUmbilical vein endothelial cellsPromising therapeutic potentialBcl-2 expressionAnti-apoptotic factorsNicorandil administrationVein endothelial cells
2011
The ATP-Binding Cassette Transporter ABCG2 Protects Against Pressure Overload–Induced Cardiac Hypertrophy and Heart Failure by Promoting Angiogenesis and Antioxidant Response
Higashikuni Y, Sainz J, Nakamura K, Takaoka M, Enomoto S, Iwata H, Tanaka K, Sahara M, Hirata Y, Nagai R, Sata M. The ATP-Binding Cassette Transporter ABCG2 Protects Against Pressure Overload–Induced Cardiac Hypertrophy and Heart Failure by Promoting Angiogenesis and Antioxidant Response. Arteriosclerosis Thrombosis And Vascular Biology 2011, 32: 654-661. PMID: 22116099, DOI: 10.1161/atvbaha.111.240341.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornAntioxidantsATP Binding Cassette Transporter, Subfamily G, Member 2ATP-Binding Cassette TransportersCells, CulturedDisease Models, AnimalEndothelial CellsGenotypeGlutathioneHeart FailureHindlimbHumansHypertrophy, Left VentricularIschemiaMaleMiceMice, KnockoutMuscle, SkeletalMyocytes, CardiacNeoplasm ProteinsNeovascularization, PhysiologicOxidative StressPhenotypeRatsRats, WistarRNA InterferenceTime FactorsTransfectionVentricular FunctionVentricular RemodelingConceptsTransverse aortic constrictionWild-type micePressure overload-induced cardiac hypertrophyMicrovascular endothelial cellsOverload-induced cardiac hypertrophyCardiac hypertrophyHeart failureEndothelial cellsCassette transporter subfamily G member 2Exaggerated cardiac hypertrophyAntioxidant responseG member 2Tissue defense mechanismsSuperoxide dismutase mimeticCassette transporter ABCG2Cardiac dysfunctionImportant endogenous antioxidantPressure overloadVentricular remodelingAortic constrictionFunctional impairmentATP-Binding Cassette Transporter ABCG2Cardiomyocyte hypertrophyImpaired angiogenesisDismutase mimetic
2007
Diverse Contribution of Bone Marrow–Derived Cells to Vascular Remodeling Associated With Pulmonary Arterial Hypertension and Arterial Neointimal Formation
Sahara M, Sata M, Morita T, Nakamura K, Hirata Y, Nagai R. Diverse Contribution of Bone Marrow–Derived Cells to Vascular Remodeling Associated With Pulmonary Arterial Hypertension and Arterial Neointimal Formation. Circulation 2007, 115: 509-517. PMID: 17242277, DOI: 10.1161/circulationaha.106.655837.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, Genetically ModifiedArteriolesBone Marrow CellsBone Marrow TransplantationCapillariesCell DifferentiationDisease Models, AnimalFemoral ArteryGreen Fluorescent ProteinsHypertension, PulmonaryMaleMonocrotalinePneumonectomyPulmonary ArteryPulmonary EmbolismRatsRats, Sprague-DawleyThrombosisTunica IntimaVentricular Dysfunction, RightConceptsPulmonary arterial hypertensionArterial neointimal formationBM-derived cellsPulmonary arterial remodelingArterial hypertensionPulmonary arteriolesProtein-positive cellsSmooth muscle cellsGreen fluorescent protein-positive cellsArterial remodelingFemoral arteryBM cellsNeointimal formationBone marrowMonocrotaline-induced pulmonary arterial hypertensionRight ventricular systolic pressureMuscle cellsVascular Remodeling AssociatedVentricular systolic pressureGreen fluorescent protein (GFP) transgenic ratsSmooth muscle-like cellsSprague-Dawley ratsWire-injured femoral arteriesMuscle-like cellsPulmonary hypertension