2013
Activation of Hypoxia‐Inducible Factor‐2 in Adipocytes Results in Pathological Cardiac Hypertrophy
Lin Q, Huang Y, Booth CJ, Haase VH, Johnson RS, Simon M, Giordano FJ, Yun Z. Activation of Hypoxia‐Inducible Factor‐2 in Adipocytes Results in Pathological Cardiac Hypertrophy. Journal Of The American Heart Association 2013, 2: e000548. PMID: 24326162, PMCID: PMC3886757, DOI: 10.1161/jaha.113.000548.Peer-Reviewed Original ResearchMeSH KeywordsAdipocytesAnimalsBasic Helix-Loop-Helix Transcription FactorsCardiomegalyCytokinesDisease Models, AnimalGene Expression RegulationGenetic Predisposition to DiseaseHypoxia-Inducible Factor 1, alpha SubunitInflammation MediatorsMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMyocytes, CardiacPhenotypeSignal TransductionTime FactorsVon Hippel-Lindau Tumor Suppressor ProteinConceptsPathological cardiac hypertrophyCardiac hypertrophyHypoxia-inducible factor-2Hypoxia-signaling pathwayHypoxia-inducible factor (HIF) pathwayVon Hippel-Lindau (VHL) geneTranscription factorsUncharacterized mechanismAdipose tissueAdipocytes resultsHIF activationObesity-associated cardiomyopathyChemotactic protein-1Protein 1Activated T cellsDirect roleEssential roleCardiomyopathy-associated genesFactor 2Genetic deletionFactor pathwayUndefined mechanismDeletionNuclear factorGenes
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 muscleEndothelial Expression of β1 Integrin Is Required for Embryonic Vascular Patterning and Postnatal Vascular Remodeling
Lei L, Liu D, Huang Y, Jovin I, Shai SY, Kyriakides T, Ross RS, Giordano FJ. Endothelial Expression of β1 Integrin Is Required for Embryonic Vascular Patterning and Postnatal Vascular Remodeling. Molecular And Cellular Biology 2008, 28: 794-802. PMID: 17984225, PMCID: PMC2223431, DOI: 10.1128/mcb.00443-07.Peer-Reviewed Original ResearchConceptsVascular patterningBeta1 integrinNormal vascular patterningEmbryonic vascular patterningBeta1 subunit expressionEmbryonic deathDevelopmental time pointsPostnatal vascular remodelingSignificant functional effectsBeta1 integrin expressionBiological processesVascular developmentExpression resultsDiminished vascularizationΒ1 integrinEmbryonic day 5Vascular remodelingCell growthGene deletionBeta1 subunitBeta1 geneIntegrins
2007
Reexpression of caveolin-1 in endothelium rescues the vascular, cardiac, and pulmonary defects in global caveolin-1 knockout mice
Murata T, Lin MI, Huang Y, Yu J, Bauer PM, Giordano FJ, Sessa WC. Reexpression of caveolin-1 in endothelium rescues the vascular, cardiac, and pulmonary defects in global caveolin-1 knockout mice. Journal Of Experimental Medicine 2007, 204: 2373-2382. PMID: 17893196, PMCID: PMC2118452, DOI: 10.1084/jem.20062340.Peer-Reviewed Original ResearchConceptsPulmonary hypertensionRC miceCaveolin-1Endothelial cellsCav-1 KO miceEpithelial cellsCav-1-deficient miceSmooth muscle contractilityEndothelial NO synthase activationNitric oxide productionBronchiolar epithelial cellsNO synthase activationSmooth muscle cellsClear physiological evidenceCaveolin-1 knockout miceLack of rescueCav-1 expressionPulmonary dysfunctionPrincipal structural componentPulmonary arteryPulmonary defectsKO miceMuscle contractilityMyocardial hypertrophyAlveolar hyperplasia
2002
Corticotropin-releasing factor receptor 2 is a tonic suppressor of vascularization
Bale TL, Giordano FJ, Hickey RP, Huang Y, Nath AK, Peterson KL, Vale WW, Lee KF. Corticotropin-releasing factor receptor 2 is a tonic suppressor of vascularization. Proceedings Of The National Academy Of Sciences Of The United States Of America 2002, 99: 7734-7739. PMID: 12032352, PMCID: PMC124337, DOI: 10.1073/pnas.102187099.Peer-Reviewed Original ResearchMeSH KeywordsAngiogenesis InhibitorsAnimalsCapillariesCell DivisionCells, CulturedEndothelial Growth FactorsEndothelium, VascularGene Expression RegulationLymphokinesMiceMice, KnockoutMuscle, Smooth, VascularNeovascularization, PhysiologicReceptors, Corticotropin-Releasing HormoneVascular Endothelial Growth Factor AVascular Endothelial Growth FactorsConceptsCorticotropin-releasing factor receptor 2Smooth muscle cellsCapillary tube formationTube formationCell cycle progressionVascular endothelial growth factorFactor receptor 2Protein phosphorylationRetinoblastoma proteinCycle progressionLigand activationReceptor 2Adult neovascularizationCRFR2-deficient miceCell proliferationIschemic cardiovascular diseasePotential targetAdult vesselsQuiescent stateMuscle cellsEndothelial growth factorGrowth factorSMC proliferationWestern blotCollagen gels
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