2019
Population and Single-Cell Analysis of Human Cardiogenesis Reveals Unique LGR5 Ventricular Progenitors in Embryonic Outflow Tract
Sahara M, Santoro F, Sohlmér J, Zhou C, Witman N, Leung CY, Mononen M, Bylund K, Gruber P, Chien KR. Population and Single-Cell Analysis of Human Cardiogenesis Reveals Unique LGR5 Ventricular Progenitors in Embryonic Outflow Tract. Developmental Cell 2019, 48: 475-490.e7. PMID: 30713072, DOI: 10.1016/j.devcel.2019.01.005.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell DifferentiationCell LineCells, CulturedEmbryonic Stem CellsEndothelial CellsHeart VentriclesHuman Embryonic Stem CellsHumansLIM-Homeodomain ProteinsMice, Inbred C57BLMultipotent Stem CellsMyocardiumMyocytes, CardiacOrganogenesisReceptors, G-Protein-CoupledSingle-Cell AnalysisConceptsCardiac stem/progenitor cellsMultipotent cardiac stem/progenitor cellsCardiac developmentMammalian cardiac developmentSingle-cell RNA-seqComprehensive gene expression profilesGene expression profilesHuman embryonic stemSingle-cell analysisStem/progenitor cellsMammalian cardiogenesisHuman cardiogenesisRNA-seqMorphogenetic processesProximal outflow tractEmbryonic stemEmbryonic outflow tractExpression profilesVentricular progenitorsPutative originHuman embryonic heartCardiac cellsEmbryonic heartProgenitor cellsCardiac derivatives
2013
Deletion of angiotensin-converting enzyme 2 promotes the development of atherosclerosis and arterial neointima formation
Sahara M, Ikutomi M, Morita T, Minami Y, Nakajima T, Hirata Y, Nagai R, Sata M. Deletion of angiotensin-converting enzyme 2 promotes the development of atherosclerosis and arterial neointima formation. Cardiovascular Research 2013, 101: 236-246. PMID: 24193738, DOI: 10.1093/cvr/cvt245.Peer-Reviewed Original ResearchMeSH KeywordsAngiotensin IIAngiotensin-Converting Enzyme 2AnimalsAortaAortic DiseasesApolipoproteins EAtherosclerosisCell ProliferationCells, CulturedDisease Models, AnimalFemoral ArteryGene DeletionGenetic Predisposition to DiseaseInflammation MediatorsJNK Mitogen-Activated Protein KinasesMacrophagesMiceMice, Inbred C57BLMice, KnockoutMuscle, Smooth, VascularMyocytes, Smooth MuscleNeointimaPeptidyl-Dipeptidase APhenotypePlaque, AtheroscleroticProtein Kinase InhibitorsRNA InterferenceSignal TransductionTransfectionVascular System InjuriesConceptsVascular smooth muscle cellsAortic vascular smooth muscle cellsArterial neointima formationVascular diseaseACE2 deficiencyVascular lesionsEnzyme 2Neointima formationApolipoprotein E knockout miceVascular cell adhesion moleculeACE2 KO miceLarge vascular lesionsAngiotensin II levelsRenin-angiotensin systemE knockout miceAortic atherosclerotic plaquesPro-inflammatory phenotypeRole of ACE2Development of atherosclerosisInflammation-related genesArterial neointimal hyperplasiaTumor necrosis factorSmooth muscle cellsPrimary bone marrow macrophagesDeletion of angiotensin
2010
A Phosphodiesterase-5 Inhibitor Vardenafil Enhances Angiogenesis Through a Protein Kinase G-Dependent Hypoxia-Inducible Factor-1/Vascular Endothelial Growth Factor Pathway
Sahara M, Sata M, Morita T, Nakajima T, Hirata Y, Nagai R. A Phosphodiesterase-5 Inhibitor Vardenafil Enhances Angiogenesis Through a Protein Kinase G-Dependent Hypoxia-Inducible Factor-1/Vascular Endothelial Growth Factor Pathway. Arteriosclerosis Thrombosis And Vascular Biology 2010, 30: 1315-1324. PMID: 20413734, DOI: 10.1161/atvbaha.109.201327.Peer-Reviewed Original ResearchMeSH KeywordsAngiogenesis Inducing AgentsAnimalsCapillariesCell HypoxiaCell MovementCells, CulturedCollateral CirculationCyclic GMPCyclic GMP-Dependent Protein KinasesCyclic Nucleotide Phosphodiesterases, Type 5Disease Models, AnimalEndothelial CellsGreen Fluorescent ProteinsHindlimbHumansHypoxia-Inducible Factor 1, alpha SubunitImidazolesIschemiaMaleMiceMice, Inbred C3HMice, Inbred C57BLMice, KnockoutMice, TransgenicMuscle, SkeletalNeovascularization, PhysiologicNitric Oxide Synthase Type IIIPhosphodiesterase 5 InhibitorsPhosphodiesterase InhibitorsPiperazinesRecovery of FunctionRegional Blood FlowRNA InterferenceSignal TransductionStem CellsSulfonesTime FactorsTransfectionTriazinesVardenafil DihydrochlorideVascular Endothelial Growth Factor AConceptsEndothelial progenitor cellsVascular endothelial growth factor (VEGF) pathwayEndothelial growth factor pathwayIschemia-induced angiogenesisGrowth factor pathwaysIschemic muscleMobilization of EPCsSca-1/flkFactor pathwaySoluble guanylate cyclase inhibitorEndothelial nitric oxide synthasePhosphodiesterase-5 inhibitor vardenafilRight femoral arteryBlood flow recoveryEffect of vardenafilPhosphodiesterase-5 inhibitionUnilateral hindlimb ischemiaGuanylate cyclase inhibitorVascular endothelial growth factorNitric oxide synthaseUpregulated protein expressionProtein kinase G inhibitorIschemic cardiovascular diseaseCapillary-like tube formationEndothelial growth factor
2005
Comparison of Various Bone Marrow Fractions in the Ability to Participate in Vascular Remodeling After Mechanical Injury
Sahara M, Sata M, Matsuzaki Y, Tanaka K, Morita T, Hirata Y, Okano H, Nagai R. Comparison of Various Bone Marrow Fractions in the Ability to Participate in Vascular Remodeling After Mechanical Injury. Stem Cells 2005, 23: 874-878. PMID: 15941860, DOI: 10.1634/stemcells.2005-0012.Peer-Reviewed Original ResearchConceptsHematopoietic stem cellsGreen fluorescent proteinGFP-positive cellsBone marrow cellsTotal bone marrow cellsMarrow cellsFluorescent proteinCell typesBone marrow fractionLin- cellsSca-1Stem cellsVascular cellsMechanical injuryMarrow fractionsCellsHSC cellsBroad potentialBone marrow reconstitutionPluripotencyVascular remodelingLesion formationRecent reportsProteinTransdifferentiation