2024
De Novo Elastin Assembly Alleviates Development of Supravalvular Aortic Stenosis—Brief Report
Ellis M, Riaz M, Huang Y, Anderson C, Hoareau M, Li X, Luo H, Lee S, Park J, Luo J, Batty L, Huang Q, Lopez C, Reinhardt D, Tellides G, Qyang Y. De Novo Elastin Assembly Alleviates Development of Supravalvular Aortic Stenosis—Brief Report. Arteriosclerosis Thrombosis And Vascular Biology 2024, 44: 1674-1682. PMID: 38752350, PMCID: PMC11209776, DOI: 10.1161/atvbaha.124.320790.Peer-Reviewed Original ResearchSupravalvular aortic stenosisVascular smooth muscle cellsSmooth muscle cellsMuscle cellsAortic stenosisMedial vascular smooth muscle cellsVascular proliferative diseasesEpigallocatechin gallate treatmentProliferative abnormalitiesPreclinical findingsHeart failureLuminal occlusionMouse modelCell hyperproliferationDefective elastinProliferative diseasesCardiovascular disordersFormation of elastinTherapeutic interventionsElastin assemblyElastin depositionStenosisMiceAortic mechanicsImproper formation
2016
Endothelial Nogo-B regulates sphingolipid biosynthesis to promote the transition from hypertrophy to heart failure during chronic pressure overload
Zhang Y, Huang Y, Cantalupo A, Azevedo P, Siragusa M, Giordano F, Di Lorenzo A. Endothelial Nogo-B regulates sphingolipid biosynthesis to promote the transition from hypertrophy to heart failure during chronic pressure overload. International Journal Of Cardiology Cardiovascular Risk And Prevention 2016, 10: e2. DOI: 10.1016/j.jash.2016.03.006.Peer-Reviewed Original Research
2012
A Designed Zinc-finger Transcriptional Repressor of Phospholamban Improves Function of the Failing Heart
Zhang HS, Liu D, Huang Y, Schmidt S, Hickey R, Guschin D, Su H, Jovin IS, Kunis M, Hinkley S, Liang Y, Hinh L, Spratt SK, Case CC, Rebar EJ, Ehrlich BE, Ehrlich B, Gregory P, Giordano F. A Designed Zinc-finger Transcriptional Repressor of Phospholamban Improves Function of the Failing Heart. Molecular Therapy 2012, 20: 1508-1515. PMID: 22828502, PMCID: PMC3412484, DOI: 10.1038/mt.2012.80.Peer-Reviewed Original ResearchConceptsHeart failureZinc finger protein transcription factorsSingle gene regulationZinc finger transcriptional repressorDiverse DNA sequencesProtein transcription factorsDisease-related genesDisease-related proteinsGene repressionZFP TFsTranscriptional repressorTranscription factorsDNA sequencesPotent repressionPLN expressionHuman diseasesRepressorContractile functionDrug targetsFailing HeartTherapeutic inhibitionAnimal modelsReuptake kineticsRepressionTherapeutic interventionsmiR-1 mediated suppression of Sorcin regulates myocardial contractility through modulation of Ca2+ signaling
Ali R, Huang Y, Maher SE, Kim RW, Giordano FJ, Tellides G, Geirsson A. miR-1 mediated suppression of Sorcin regulates myocardial contractility through modulation of Ca2+ signaling. Journal Of Molecular And Cellular Cardiology 2012, 52: 1027-1037. PMID: 22326846, DOI: 10.1016/j.yjmcc.2012.01.020.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBase SequenceCalcium SignalingCalcium-Binding ProteinsCardiac VolumeCardiomyopathiesCell LineDEAD-box RNA HelicasesHeartHumansMaleMiceMice, 129 StrainMice, Inbred C57BLMice, KnockoutMicroRNAsMyocardial ContractionMyocardiumRibonuclease IIIRNA InterferenceRNA, Small InterferingUp-RegulationConceptsCardiac functionMiR-1Normal cardiac contractile functionEnd-stage cardiomyopathyCardiac contractile functionWild-type miceCalcium signalingExcitation-contraction couplingModulation of Ca2Cultured mouse cardiomyocytesAcute cardiomyopathyMiR-1 targetsHeart failureMyocardial contractilityMiR-1 knockdownContractile functionAntagomir treatmentSorcin expressionCalcium homeostasisKnockdown miceSorcin levelsCardiac phenotypeMouse cardiomyocytesCritical mediatorPathological relevance
2008
Hypoxia-Inducible Factor-Dependent Degeneration, Failure, and Malignant Transformation of the Heart in the Absence of the von Hippel-Lindau Protein
Lei L, Mason S, Liu D, Huang Y, Marks C, Hickey R, Jovin IS, Pypaert M, Johnson RS, Giordano FJ. Hypoxia-Inducible Factor-Dependent Degeneration, Failure, and Malignant Transformation of the Heart in the Absence of the von Hippel-Lindau Protein. Molecular And Cellular Biology 2008, 28: 3790-3803. PMID: 18285456, PMCID: PMC2423296, DOI: 10.1128/mcb.01580-07.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCapillariesCell Transformation, NeoplasticErbB ReceptorsGene DeletionGene Transfer TechniquesHeart FailureHeart NeoplasmsHypoxiaHypoxia-Inducible Factor 1, alpha SubunitLipid MetabolismLipidsMiceMice, KnockoutMyocardiumNeovascularization, PhysiologicPhosphorylationProto-Oncogene Proteins c-metRas ProteinsVon Hippel-Lindau Tumor Suppressor ProteinConceptsHeart failureVon Hippel-Lindau proteinChronic activationAdvanced ischemic heart diseaseMalignant cardiac tumorsHIF-1alphaProgressive heart failureIschemic heart diseaseCardiac myocyte-specific deletionHIF pathwayHuman heart failureFeatures of rhabdomyosarcomaHypoxia-inducible factorHypoxia-inducible transcription factor-1Cardiac tumorsHeart diseaseTranscription factor 1Cardiac degenerationIschemic heartMyocyte lossDependent degenerationMalignant transformationPremature deathLipid accumulationCardiac muscleChromogranin B Regulates Calcium Signaling, Nuclear Factor &kgr;B Activity, and Brain Natriuretic Peptide Production in Cardiomyocytes
Heidrich FM, Zhang K, Estrada M, Huang Y, Giordano FJ, Ehrlich BE. Chromogranin B Regulates Calcium Signaling, Nuclear Factor &kgr;B Activity, and Brain Natriuretic Peptide Production in Cardiomyocytes. Circulation Research 2008, 102: 1230-1238. PMID: 18420944, PMCID: PMC2952358, DOI: 10.1161/circresaha.107.166033.Peer-Reviewed Original ResearchMeSH KeywordsAge FactorsAngiotensin IIAnimalsCalciumCalcium SignalingCardiomegalyCells, CulturedChromogranin BInositol 1,4,5-Trisphosphate ReceptorsMyocytes, CardiacNatriuretic Peptide, BrainNFATC Transcription FactorsNF-kappa BPromoter Regions, GeneticRatsTranscription, GeneticVasoconstrictor AgentsConceptsBrain natriuretic peptideAngiotensin IICardiac hypertrophyBNP productionChromogranin BNuclear factorNuclear factor-kappaB activityNatriuretic peptide productionActivated T cellsNuclear factor-kappaBLuciferase reporter assaysHeart failureNatriuretic peptideBasal secretionCardiovascular diseaseT cellsKappaB activityFactor-kappaBHypertrophyCGB expressionBNP promoterPotent inducerAdult cardiomyocytesOctapeptide hormoneCalcium signaling