2017
Response to “Comment to the article ‘Diverse contribution of bone marrow-derived late-outgrowth endothelial progenitor cells to vascular repair under pulmonary arterial hypertension and arterial neointimal formation’”
Ikutomi M, Minami Y, Sahara M. Response to “Comment to the article ‘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 2017, 103: 137-138. PMID: 28109765, DOI: 10.1016/j.yjmcc.2017.01.010.Commentaries, Editorials and Letters
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
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