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
Urocortin2 inhibits tumor growth via effects on vascularization and cell proliferation
Hao Z, Huang Y, Cleman J, Jovin IS, Vale WW, Bale TL, Giordano FJ. Urocortin2 inhibits tumor growth via effects on vascularization and cell proliferation. Proceedings Of The National Academy Of Sciences Of The United States Of America 2008, 105: 3939-3944. PMID: 18308934, PMCID: PMC2268793, DOI: 10.1073/pnas.0712366105.Peer-Reviewed Original ResearchConceptsInhibits tumor growthTumor growthTumor vascularizationActivation of CRFR2Potential therapeutic roleTumor growth inhibitionTumor-suppressing effectsCRFR2 activationMeasurable tumorsTumor cell cyclingCell tumorsTherapeutic roleClinical malignancyUrocortin 2Peripheral tissuesCRFR2Ucn2Genetic deletionTissue vascularityDirect inhibitionVessel diameterCell proliferationVessel numberVascularizationTumorsEndothelial 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
2006
An engineered VEGF‐activating zinc finger protein transcription factor improves blood flow and limb salvage in advanced‐age mice
Yu J, Lei L, Liang Y, Hinh L, Hickey RP, Huang Y, Liu D, Yeh JL, Rebar E, Case C, Spratt K, Sessa WC, Giordano FJ. An engineered VEGF‐activating zinc finger protein transcription factor improves blood flow and limb salvage in advanced‐age mice. The FASEB Journal 2006, 20: 479-481. PMID: 16423874, DOI: 10.1096/fj.04-3670fje.Peer-Reviewed Original ResearchMeSH KeywordsAdenoviridaeAgingAmino Acid SequenceAnimalsBlood Flow VelocityFeasibility StudiesGene Expression RegulationGenes, SyntheticGenetic TherapyGenetic VectorsHindlimbIschemiaLaser-Doppler FlowmetryMiceMice, Inbred C57BLMolecular Sequence DataNeovascularization, PhysiologicProtein EngineeringRecombinant ProteinsRNA, MessengerStructure-Activity RelationshipTranscription FactorsVascular Endothelial Growth Factor AZinc FingersConceptsLimb salvageBlood flowHindlimb ischemiaC57/BL6 micePeripheral vascular diseaseVascular endothelial growth factorPotential clinical utilityEndothelial growth factorExpression of VEGFABL6 miceIschemic limbsVascular diseaseIschemic hindlimbMurine modelClinical utilityVessel countProtein transcription factorsGrowth factorProtein levelsSalvage