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
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
2010
The ATP-Binding Cassette Transporter BCRP1/ABCG2 Plays a Pivotal Role in Cardiac Repair After Myocardial Infarction Via Modulation of Microvascular Endothelial Cell Survival and Function
Higashikuni Y, Sainz J, Nakamura K, Takaoka M, Enomoto S, Iwata H, Sahara M, Tanaka K, Koibuchi N, Ito S, Kusuhara H, Sugiyama Y, Hirata Y, Nagai R, Sata M. The ATP-Binding Cassette Transporter BCRP1/ABCG2 Plays a Pivotal Role in Cardiac Repair After Myocardial Infarction Via Modulation of Microvascular Endothelial Cell Survival and Function. Arteriosclerosis Thrombosis And Vascular Biology 2010, 30: 2128-2135. PMID: 20829509, DOI: 10.1161/atvbaha.110.211755.Peer-Reviewed Original ResearchConceptsBreast cancer resistance protein 1BCRP1/ABCG2Myocardial infarctionWT miceCardiac repairEndothelial cellsEndothelial cell survivalAbcg2 knockout micePeri-infarction areaMember 2 expressionTissue defense mechanismsMicrovascular endothelial cellsCell survivalResistance protein 1Cardiac ruptureIntracellular protoporphyrin IXVentricular remodelingKO micePivotal roleHistological assessmentKnockout miceSurvival rateABCG2 inhibitionMiceOxidative stressA 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