2012
miR-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 muscle
2004
Stromal Cell–Derived Factor-1α Plays a Critical Role in Stem Cell Recruitment to the Heart After Myocardial Infarction but Is Not Sufficient to Induce Homing in the Absence of Injury
Abbott JD, Huang Y, Liu D, Hickey R, Krause DS, Giordano FJ. Stromal Cell–Derived Factor-1α Plays a Critical Role in Stem Cell Recruitment to the Heart After Myocardial Infarction but Is Not Sufficient to Induce Homing in the Absence of Injury. Circulation 2004, 110: 3300-3305. PMID: 15533866, DOI: 10.1161/01.cir.0000147780.30124.cf.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBenzylaminesBone Marrow CellsBone Marrow TransplantationCell LineageCell MovementChemokine CXCL12Chemokines, CXCCyclamsFemaleGene Expression ProfilingGene Expression RegulationGenetic TherapyHeterocyclic CompoundsIntercellular Adhesion Molecule-1Matrix Metalloproteinase 9MiceMice, Inbred NODMice, SCIDMyocardial InfarctionMyocardiumReceptors, CXCR4Recombinant Fusion ProteinsStem Cell TransplantationStem CellsTransduction, GeneticVascular Cell Adhesion Molecule-1Vascular Endothelial Growth Factor AConceptsBone marrow-derived cellsStromal cell-derived factor-1alphaMyocardial infarctionBMDC recruitmentAdhesion molecule-1Molecule-1Recruitment of BMDCsInfarcted heartSerum SDF-1 levelsVascular cell adhesion molecule-1Intercellular adhesion molecule-1Stromal cell-derived factor-1αCell adhesion molecule-1Administration of AMD3100SDF-1/CXCR4 interactionMarrow-derived cellsSDF-1 levelsAbsence of MIVascular endothelial growth factorMatrix metalloproteinase-9Sham-operated controlsSDF-1 mRNAEndothelial growth factorAbsence of injuryQuantitative polymerase chain reaction
2001
A cardiac myocyte vascular endothelial growth factor paracrine pathway is required to maintain cardiac function
Giordano F, Gerber H, Williams S, VanBruggen N, Bunting S, Ruiz-Lozano P, Gu Y, Nath A, Huang Y, Hickey R, Dalton N, Peterson K, Ross J, Chien K, Ferrara N. A cardiac myocyte vascular endothelial growth factor paracrine pathway is required to maintain cardiac function. Proceedings Of The National Academy Of Sciences Of The United States Of America 2001, 98: 5780-5785. PMID: 11331753, PMCID: PMC33290, DOI: 10.1073/pnas.091415198.Peer-Reviewed Original ResearchConceptsBasal contractile functionCardiac myocyte-specific deletionAdult murine modelCardiac contractile dysfunctionVascular endothelial growth factorBeta-adrenergic stimulationCardiomyocyte-specific knockoutEndothelial growth factorVascular endothelial growth factor (VEGF) geneContractile dysfunctionCardiac functionContractile functionCoronary microvesselsAbnormal responseMurine modelHeart functionParacrine pathwaysGrowth factor geneVentricular wallGrowth factorCardiac myocytesHypoxia-responsive genesEnergy metabolismMiceHeart