2000
Basic FGF reduces stunning via a NOS2-dependent pathway in coronary-perfused mouse hearts
Hampton T, Amende I, Fong J, Laubach V, Li J, Metais C, Simons M. Basic FGF reduces stunning via a NOS2-dependent pathway in coronary-perfused mouse hearts. AJP Heart And Circulatory Physiology 2000, 279: h260-h268. PMID: 10899065, DOI: 10.1152/ajpheart.2000.279.1.h260.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCalciumCoronary VesselsEnzyme InhibitorsFemaleFibroblast Growth Factor 2HeartIn Vitro TechniquesLysineMaleMiceMice, Inbred C57BLMice, KnockoutMyocardial IschemiaMyocardial ReperfusionMyocardial StunningNG-Nitroarginine Methyl EsterNitric Oxide SynthaseNitric Oxide Synthase Type IIRecombinant ProteinsConceptsFGF-2Mouse heartsBasic FGFIschemia-reperfusion injuryExpression of NOS2Onset of ischemiaInducible NO synthaseBasic fibroblast growth factorNitric oxide productionNO-selective electrodeFibroblast growth factorLV dysfunctionIschemic contractureVentricular functionLV recoveryNO synthaseIntracellular calciumProtective effectTransgenic heartsOxide productionIschemiaGrowth factorReperfusionSelective inhibitorVehicle controlPR39, a peptide regulator of angiogenesis
Li J, Post M, Volk R, Gao Y, Li M, Metais C, Sato K, Tsai J, Aird W, Rosenberg R, Hampton T, Li J, Sellke F, Carmeliet P, Simons M. PR39, a peptide regulator of angiogenesis. Nature Medicine 2000, 6: 49-55. PMID: 10613823, DOI: 10.1038/71527.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntimicrobial Cationic PeptidesAortaCapillariesCattleCell HypoxiaCells, CulturedCoronary VesselsCysteine EndopeptidasesDNA-Binding ProteinsEndothelium, VascularHeartHumansHypoxia-Inducible Factor 1Hypoxia-Inducible Factor 1, alpha SubunitIn Vitro TechniquesMacrophagesMiceMice, Inbred C57BLMice, TransgenicMultienzyme ComplexesMyocardial InfarctionMyocardial IschemiaNeovascularization, PhysiologicNuclear ProteinsPeptidesProteasome Endopeptidase ComplexRecombinant ProteinsSwineTranscription FactorsUbiquitinsUmbilical VeinsVon Willebrand FactorConceptsHypoxia-inducible factor-1α (HIF-1α) degradationMacrophage-derived peptideHypoxia-inducible factor-1α (HIF-1α) proteinCoronary flow studiesInflammation-induced angiogenesisInduction of angiogenesisMyocardial vasculatureTissue injuryPotent inductorFunctional blood vesselsBlood vesselsVascular structuresAngiogenesisSelective inhibitionPR39
1998
Effects of coronary artery disease on expression and microvascular response to VEGF
Métais C, Li J, Li J, Simons M, Sellke F. Effects of coronary artery disease on expression and microvascular response to VEGF. American Journal Of Physiology 1998, 275: h1411-h1418. PMID: 9746492, DOI: 10.1152/ajpheart.1998.275.4.h1411.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine DiphosphateCell DivisionCoronary Artery BypassCoronary DiseaseEndothelial Growth FactorsEndothelium, VascularFemaleGene Expression RegulationGenisteinHeart AtriaHepatocyte Growth FactorHumansIn Vitro TechniquesKineticsLymphokinesMaleMicrocirculationMicroscopy, VideoMiddle AgedMuscle RelaxationMuscle, Smooth, VascularNitric Oxide SynthaseNitric Oxide Synthase Type IINitric Oxide Synthase Type IIINitroarginineProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesReceptors, Growth FactorReceptors, MitogenReceptors, Vascular Endothelial Growth FactorRNA, MessengerTranscription, GeneticVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth FactorsVasodilationConceptsCoronary artery diseaseInducible nitric oxide synthaseConstitutive nitric oxide synthaseVascular endothelial growth factorHepatocyte growth factorExpression of VEGFNitric oxide synthaseArtery diseaseNG-nitroMicrovascular responsesOxide synthaseExpression of cNOSL-arginineGrowth factorCoronary microvascular responsesSubstance P responseExogenous vascular endothelial growth factorEndothelial growth factorFlk-1 receptorFlt-1 receptorMild hypercholesterolemiaTyrosine kinase receptorsTyrosine kinase inhibitor genisteinEndothelium dysfunctionVascular responses