2023
STRA6 is essential for induction of vascular smooth muscle lineages in human embryonic cardiac outflow tract development
Zhou C, Häneke T, Rohner E, Sohlmér J, Kameneva P, Artemov A, Adameyko I, Sahara M. STRA6 is essential for induction of vascular smooth muscle lineages in human embryonic cardiac outflow tract development. Cardiovascular Research 2023, 119: 1202-1217. PMID: 36635482, PMCID: PMC10202647, DOI: 10.1093/cvr/cvad010.Peer-Reviewed Original ResearchConceptsHuman embryonic stem cellsHuman cardiogenesisWild-type human embryonic stem cellsSmooth muscle cellsCardiac outflow tract developmentSingle-cell RNA sequencing datasetsRARα/RXRαCardiogenic transcription factorsRNA sequencing datasetsSmooth muscle lineageRetinoic acid signalingEmbryonic stem cellsVascular smooth muscle lineageRNA-seq dataOutflow tract developmentCardiac outflow tractOFT formationHeart progenitorsMuscle lineageSTRA6 mutationsRas signalingMurine embryonic heartTranscription factorsAcid signalingHeart development
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
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