2019
Angiotensin Receptor Neprilysin Inhibitor Attenuates Myocardial Remodeling and Improves Infarct Perfusion in Experimental Heart Failure
Pfau D, Thorn SL, Zhang J, Mikush N, Renaud JM, Klein R, deKemp RA, Wu X, Hu X, Sinusas AJ, Young LH, Tirziu D. Angiotensin Receptor Neprilysin Inhibitor Attenuates Myocardial Remodeling and Improves Infarct Perfusion in Experimental Heart Failure. Scientific Reports 2019, 9: 5791. PMID: 30962467, PMCID: PMC6453892, DOI: 10.1038/s41598-019-42113-0.Peer-Reviewed Original ResearchMeSH KeywordsAminobutyratesAngiotensin Receptor AntagonistsAnimalsBiphenyl CompoundsDrug CombinationsHeartHeart FailureMaleMyocardial Reperfusion InjuryMyocardiumNeovascularization, PhysiologicNeprilysinOrganotechnetium CompoundsPeptides, CyclicRatsRats, Inbred LewSingle Photon Emission Computed Tomography Computed TomographyTetrazolesValsartanVascular Endothelial Growth Factor AVentricular RemodelingConceptsSacubitril/valsartanExperimental heart failureHeart failureMyocardial infarctionMyocardial remodelingAngiotensin receptor neprilysin inhibitorAngiotensin receptor blocker valsartanMicroSPECT/CT imagingReceptor blocker valsartanHeart failure patientsProgressive LV dilationGlobal LV functionLV contractile dysfunctionNeprilysin inhibitor sacubitrilBorder zoneLimited remodelingFailure patientsInhibitor therapyMale LewisWeeks treatmentLV dilationLV functionNeprilysin inhibitorContractile dysfunctionInterstitial fibrosis
2014
Live cell imaging of primary rat neonatal cardiomyocytes following adenoviral and lentiviral transduction using confocal spinning disk microscopy.
Sakurai T, Lanahan A, Woolls MJ, Li N, Tirziu D, Murakami M. Live cell imaging of primary rat neonatal cardiomyocytes following adenoviral and lentiviral transduction using confocal spinning disk microscopy. Journal Of Visualized Experiments 2014, e51666. PMID: 24998400, PMCID: PMC4209952, DOI: 10.3791/51666.Peer-Reviewed Original ResearchConceptsRat neonatal cardiomyocytesConfocal spinning disk microscopyLive cell imagesFunction of genesConfocal spinning disk microscopeNeonatal cardiomyocytesPrimary rat neonatal cardiomyocytesCultured primary cellsUse of siRNAsDisk microscopyDifferent genesChemical modulatorsCellular eventsDisk microscopePrimary cellsLentiviral transductionExpression levelsAdenoviral transductionCell imagingTransductionGenesTransduction ratesMicroscope technologyCellsCardiomyocytes
2013
NO triggers RGS4 degradation to coordinate angiogenesis and cardiomyocyte growth
Jaba IM, Zhuang ZW, Li N, Jiang Y, Martin KA, Sinusas AJ, Papademetris X, Simons M, Sessa WC, Young LH, Tirziu D. NO triggers RGS4 degradation to coordinate angiogenesis and cardiomyocyte growth. Journal Of Clinical Investigation 2013, 123: 1718-1731. PMID: 23454748, PMCID: PMC3613910, DOI: 10.1172/jci65112.Peer-Reviewed Original ResearchMeSH KeywordsAdaptation, BiologicalAnimalsCell EnlargementCells, CulturedCoronary VesselsEndothelium, VascularHeart VentriclesMechanistic Target of Rapamycin Complex 1MiceMice, Inbred C57BLMice, TransgenicMultiprotein ComplexesMyocytes, CardiacNeovascularization, PhysiologicNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide SynthasePlacenta Growth FactorPregnancy ProteinsProteinsProteolysisProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleyRGS ProteinsSignal TransductionTOR Serine-Threonine KinasesConceptsCardiomyocyte growthAkt/mTORC1 signalingNovel NO-dependent mechanismProteasomal degradationCoordination of angiogenesisMTORC1 signalingConditional overexpressionMurine cardiac tissueG proteinsTransgenic expressionAkt/Physiological mechanismsMyocyte growthVessel growthGrowth factorTransgenic miceHypertrophic responseAngiogenesisKnockout miceMyocardial hypertrophyExpressionGrowthCardiac hypertrophyNOS inhibitor L-NAMEInduction
2007
Myocardial hypertrophy in the absence of external stimuli is induced by angiogenesis in mice
Tirziu D, Chorianopoulos E, Moodie KL, Palac RT, Zhuang ZW, Tjwa M, Roncal C, Eriksson U, Fu Q, Elfenbein A, Hall AE, Carmeliet P, Moons L, Simons M. Myocardial hypertrophy in the absence of external stimuli is induced by angiogenesis in mice. Journal Of Clinical Investigation 2007, 117: 3188-3197. PMID: 17975666, PMCID: PMC2045601, DOI: 10.1172/jci32024.Peer-Reviewed Original ResearchMeSH KeywordsAngiogenic ProteinsAnimalsCardiomegalyCells, CulturedEchocardiographyEndothelial CellsEnzyme InhibitorsHeartHemodynamicsMiceMice, Inbred C57BLMice, TransgenicMyocardiumMyocytes, CardiacNeovascularization, PhysiologicNG-Nitroarginine Methyl EsterOrgan SizeRatsRats, Sprague-DawleyTransgenesConceptsMyocardial hypertrophyHeart sizeNormal heart sizeENOS inhibitor L-NAMEInhibitor L-NAMEAtrial natriuretic factorHypertrophic marker expressionNormal adult mouse heartAdult mouse heartAngiogenic growth factorsL-NAMEBeta-MHCCardiac massMyocardial infarctionMyocardial functionNatriuretic factorCardiac performanceCardiomyocyte sizeTransgenic miceStimulation periodHeart growthHypertrophy markersMarker expressionMouse heartsMurine heart
1996
Increased macrophage uptake of irreversibly glycated albumin modified-low density lipoproteins of normal and diabetic subjects is mediated by non-saturable mechanisms
Dobrian A, Lazar V, Tirziu D, Simionescu M. Increased macrophage uptake of irreversibly glycated albumin modified-low density lipoproteins of normal and diabetic subjects is mediated by non-saturable mechanisms. Biochimica Et Biophysica Acta 1996, 1317: 5-14. PMID: 8876621, DOI: 10.1016/0925-4439(96)00017-8.Peer-Reviewed Original ResearchConceptsAGE-AlbAdvanced glycosylation end productsDiabetic subjectsDensity lipoproteinAGE-albuminModified-low density lipoproteinsMacrophage uptakeOxidative-antioxidative balanceIndependent risk factorNon-saturable pathwayLow-density lipoproteinNon-saturable mechanismReceptor-mediated uptakeGlycosylation end productsLevel of glycationDiabetes mellitusDiabetic stateRisk factorsAtherosclerotic plaquesLipid peroxidesAcetylated LDLPeritoneal macrophagesReceptor pathwayLipoproteinDLDL