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
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 reactionLoss of HIF-1α in endothelial cells disrupts a hypoxia-driven VEGF autocrine loop necessary for tumorigenesis
Tang N, Wang L, Esko J, Giordano FJ, Huang Y, Gerber HP, Ferrara N, Johnson RS. Loss of HIF-1α in endothelial cells disrupts a hypoxia-driven VEGF autocrine loop necessary for tumorigenesis. Cancer Cell 2004, 6: 485-495. PMID: 15542432, DOI: 10.1016/j.ccr.2004.09.026.Peer-Reviewed Original ResearchAnimalsCell HypoxiaCell ProliferationCells, CulturedChemotaxisEndothelial CellsGene Expression RegulationHypoxia-Inducible Factor 1, alpha SubunitMiceNeoplasmsNeovascularization, PathologicTranscription FactorsVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2Wound Healing
2002
Induction of angiogenesis in a mouse model using engineered transcription factors
Rebar EJ, Huang Y, Hickey R, Nath AK, Meoli D, Nath S, Chen B, Xu L, Liang Y, Jamieson AC, Zhang L, Spratt SK, Case CC, Wolffe A, Giordano FJ. Induction of angiogenesis in a mouse model using engineered transcription factors. Nature Medicine 2002, 8: 1427-1432. PMID: 12415262, DOI: 10.1038/nm1202-795.Peer-Reviewed Original ResearchMeSH Keywords3T3 CellsAmino Acid SequenceAngiogenesis Inducing AgentsAnimalsDrug DesignGene Expression RegulationGenetic TherapyMiceModels, AnimalMolecular Sequence DataNeovascularization, PhysiologicProtein EngineeringRecombinant ProteinsTranscription FactorsVascular Endothelial Growth Factor AZinc FingersConceptsTranscription factorsEndogenous genesZinc finger protein transcription factorsProtein transcription factorsWhole-organism modelDNA sequencesInduced expressionGenesInduction of angiogenesisZFPExpression of VEGFAProtein VEGFExpressionGrowth factorStimulation of angiogenesisTissue cultureVascular endothelial growth factorExperimental wound healingEndothelial growth factorWound healingNatural arraysAngiogenesisVivoCDNAMouse modelCorticotropin-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 ResearchMeSH KeywordsAnimalsEndothelial Growth FactorsGene Expression ProfilingHeartImmunohistochemistryIn Situ HybridizationLymphokinesMiceMice, KnockoutModels, AnimalMyocardiumVascular Endothelial Growth Factor AVascular Endothelial Growth FactorsConceptsBasal 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