2017
MMP-2: A modulator of neuronal precursor activity and cognitive and motor behaviors
Li Q, Michaud M, Shankar R, Canosa S, Schwartz M, Madri JA. MMP-2: A modulator of neuronal precursor activity and cognitive and motor behaviors. Behavioural Brain Research 2017, 333: 74-82. PMID: 28666838, DOI: 10.1016/j.bbr.2017.06.041.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornCell MovementCell ProliferationCells, CulturedCognitionExploratory BehaviorGene Expression RegulationMatrix Metalloproteinase 2MiceMice, Inbred C57BLMice, KnockoutMotor ActivityNerve Tissue ProteinsNeural Stem CellsNeurogenesisOncogene Protein v-aktProliferating Cell Nuclear AntigenReceptors, CXCR4Spatial LearningConceptsNeural precursor cellsBroad substrate specificityNeurosphere formationAdherent neurospheresSecondary neurosphere formationNPC activitySubstrate specificityNPC numberCell surface moleculesZinc-containing enzymesAkt activationAbsence of MMP2Cell typesExtracellular matrixActivity assaysPrecursor cellsImportant roleNPC migrationMatrix metalloproteinase2Surface moleculesExpressionKO miceBioactive moleculesNestin expressionMMP2The role of endothelial HIF-1 αin the response to sublethal hypoxia in C57BL/6 mouse pups
Li Q, Michaud M, Park C, Huang Y, Couture R, Girodano F, Schwartz ML, Madri JA. The role of endothelial HIF-1 αin the response to sublethal hypoxia in C57BL/6 mouse pups. Laboratory Investigation 2017, 97: 356-369. PMID: 28092362, DOI: 10.1038/labinvest.2016.154.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornApoptosisBlotting, WesternCell HypoxiaCell ProliferationCells, CulturedDentate GyrusEndothelial CellsFemaleHypoxiaHypoxia-Inducible Factor 1, alpha SubunitLateral VentriclesMaleMice, Inbred C57BLMice, KnockoutMice, TransgenicMicroscopy, FluorescenceMotor ActivityNeural Stem CellsConceptsHIF-1 αBrain microvascular endothelial cellsNeuronal precursor cellsSubventricular zoneMicrovascular endothelial cellsOpen-field activityEndothelial cellsSublethal hypoxiaHIF-1 α expressionOpen-field activity testChronic sublethal hypoxiaEndothelial HIF-1Hypoxic conditionsC57BL/6 mouse pupsGender-specific differencesPremature birthC57BL/6 WTDentate gyrusHippocampal tissueDeficient miceΑ expressionMouse pupsMotor handicapParacrine effectsDentate gyrus tissue
2015
A hydrogel-endothelial cell implant mimics infantile hemangioma: modulation by survivin and the Hippo pathway
Tsuneki M, Hardee S, Michaud M, Morotti R, Lavik E, Madri JA. A hydrogel-endothelial cell implant mimics infantile hemangioma: modulation by survivin and the Hippo pathway. Laboratory Investigation 2015, 95: 765-780. PMID: 25961170, PMCID: PMC4828971, DOI: 10.1038/labinvest.2015.61.Peer-Reviewed Original ResearchAdaptor Proteins, Signal TransducingAnimalsCell Cycle ProteinsCells, CulturedChildChild, PreschoolDisease Models, AnimalEndothelial CellsFemaleHemangiomaHumansHydrogel, Polyethylene Glycol DimethacrylateInfantInhibitor of Apoptosis ProteinsLIM Domain ProteinsMacrophagesMaleMice, Inbred C57BLPhosphoproteinsRepressor ProteinsSurvivinTissue Array AnalysisTissue ScaffoldsYAP-Signaling Proteins
2014
Stratified control of IGF-I expression by hypoxia and stress hormones in osteoblasts
McCarthy TL, Yun Z, Madri JA, Centrella M. Stratified control of IGF-I expression by hypoxia and stress hormones in osteoblasts. Gene 2014, 539: 141-151. PMID: 24440782, PMCID: PMC4316208, DOI: 10.1016/j.gene.2014.01.011.Peer-Reviewed Original ResearchMeSH KeywordsAlkaline PhosphataseAnimalsCCAAT-Enhancer-Binding Protein-deltaCell HypoxiaCells, CulturedCore Binding Factor Alpha 1 SubunitDinoprostoneDNADNA ReplicationGene Expression RegulationHydrocortisoneInsulin-Like Growth Factor IOsteoblastsOxygenPromoter Regions, GeneticProtein BiosynthesisRatsRats, Sprague-DawleyRegulatory Elements, TranscriptionalRNA, MessengerConceptsIGF-I expressionStress hormonesIGF-I gene promoterIGF-I mRNAInfluence of PGE2Transcription factor C/EBPδOsteoblast transcription factor Runx2Hypoxic inhibitionI expressionPGE2Stimulatory effectGlucocorticoidsHypoxiaHIF activityHypoxic stressTranscription factor Runx2Bone cellsIGFProlonged exposureHormoneAlkaline phosphatase activitySystemic regulationOsteoblastsResponse elementRunx2CD44 Regulation of Endothelial Cell Proliferation and Apoptosis via Modulation of CD31 and VE-cadherin Expression*
Tsuneki M, Madri JA. CD44 Regulation of Endothelial Cell Proliferation and Apoptosis via Modulation of CD31 and VE-cadherin Expression*. Journal Of Biological Chemistry 2014, 289: 5357-5370. PMID: 24425872, PMCID: PMC3937614, DOI: 10.1074/jbc.m113.529313.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, CDApoptosisCadherinsCell AdhesionCell ProliferationCells, CulturedEndothelial CellsGene Expression RegulationHippo Signaling PathwayHyaluronan ReceptorsInhibitor of Apoptosis ProteinsMiceMice, KnockoutPlatelet Endothelial Cell Adhesion Molecule-1Protein Serine-Threonine KinasesProtein Structure, TertiaryRepressor ProteinsSurvivinConceptsVE-cadherin expressionHippo pathwayYAP nuclear localizationCortical membrane proteinsAdhesion protein expressionInitiator caspasesMembrane proteinsNuclear localizationCaspase cascadeEndothelial cellsHigh cell densityCritical regulatorCD44 regulationJunctional integrityKey roleCell behaviorEndothelial cell proliferationCell growthDiverse arrayCell proliferationVascular barrier integrityProtein expressionRole of CD44Pathway activationMurine CD44
2012
Short Term Interactions with Long Term Consequences: Modulation of Chimeric Vessels by Neural Progenitors
Williams C, Rauch MF, Michaud M, Robinson R, Xu H, Madri J, Lavik E. Short Term Interactions with Long Term Consequences: Modulation of Chimeric Vessels by Neural Progenitors. PLOS ONE 2012, 7: e53208. PMID: 23300890, PMCID: PMC3531360, DOI: 10.1371/journal.pone.0053208.Peer-Reviewed Original Research
2011
Varying Effects of Hemodynamic Forces on Tissue Factor RNA Expression in Human Endothelial Cells
Abe R, Yamashita N, Rochier A, Nixon A, Abe R, Madri JA, Sumpio BE. Varying Effects of Hemodynamic Forces on Tissue Factor RNA Expression in Human Endothelial Cells. Journal Of Surgical Research 2011, 170: 150-156. PMID: 21592524, DOI: 10.1016/j.jss.2011.04.002.Peer-Reviewed Original ResearchConceptsLaminar flowOscillatory flowCyclic strainUnidirectional laminar flowUniform laminar flowMechanical stressDisturbed flowTF RNA expressionHuman umbilical vein endothelial cellsFlowStatic controlHigh TF expressionTF expressionForceMechanical forcesEndothelial cellsRNA expressionSustained amplificationLaminar shear, but not orbital shear, has a synergistic effect with thrombin stimulation on tissue factor expression in human umbilical vein endothelial cells
Rochier A, Nixon A, Yamashita N, Abe R, Abe R, Madri JA, Sumpio BE. Laminar shear, but not orbital shear, has a synergistic effect with thrombin stimulation on tissue factor expression in human umbilical vein endothelial cells. Journal Of Vascular Surgery 2011, 54: 480-488. PMID: 21367569, DOI: 10.1016/j.jvs.2011.01.002.Peer-Reviewed Original ResearchAnalysis of VarianceBlotting, WesternCell Culture TechniquesCells, CulturedEndothelial CellsEnzyme ActivationHumansMechanotransduction, CellularMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3P38 Mitogen-Activated Protein KinasesPhosphorylationProtein Kinase InhibitorsRNA, MessengerStress, MechanicalThrombinThromboplastinTime FactorsUp-RegulationPulsatile to-fro flow induces greater and sustained expression of tissue factor RNA in HUVEC than unidirectional laminar flow
Abe R, Yamashita N, Rochier A, Abe R, Nixon A, Madri JA, Sumpio BE. Pulsatile to-fro flow induces greater and sustained expression of tissue factor RNA in HUVEC than unidirectional laminar flow. AJP Heart And Circulatory Physiology 2011, 300: h1345-h1351. PMID: 21257914, PMCID: PMC3075035, DOI: 10.1152/ajpheart.01197.2010.Peer-Reviewed Original Research
2009
Strain Differences in Behavioral and Cellular Responses to Perinatal Hypoxia and Relationships to Neural Stem Cell Survival and Self-Renewal Modeling the Neurovascular Niche
Li Q, Liu J, Michaud M, Schwartz ML, Madri JA. Strain Differences in Behavioral and Cellular Responses to Perinatal Hypoxia and Relationships to Neural Stem Cell Survival and Self-Renewal Modeling the Neurovascular Niche. American Journal Of Pathology 2009, 175: 2133-2145. PMID: 19815710, PMCID: PMC2774076, DOI: 10.2353/ajpath.2009.090354.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBehavior, AnimalCell DifferentiationCell MovementCell SurvivalCells, CulturedChemokine CXCL12Endothelial CellsEnzyme ActivationFemaleHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitHypoxia-Inducible Factor-Proline DioxygenasesInfantInfant, NewbornInfant, PrematureMaleMiceMice, Inbred C57BLMice, Inbred StrainsNeuronsNeuropsychological TestsPhosphatidylinositol 3-KinasesProcollagen-Proline DioxygenaseProto-Oncogene Proteins c-aktSignal TransductionStem CellsConceptsChronic hypoxiaC57 miceHIF-1alphaLow birth weight infant populationMatrix metalloproteinase-9 activityStromal-derived factor-1CD-1 miceMetalloproteinase-9 activityAdult C57 miceHypoxia-induced factorNeural stem cell survivalHigher apoptosis ratePerinatal hypoxiaRepair/recoveryClinical improvementNeurodevelopmental handicapPreventive therapyPremature infantsNeurogenic zonesNeurovascular nicheInfant populationC57BL/6 pupsProlyl hydroxylase domain 2Migratory responsivenessStem cell survivalBone Marrow Monocyte PECAM-1 Deficiency Elicits Increased Osteoclastogenesis Resulting in Trabecular Bone Loss
Wu Y, Tworkoski K, Michaud M, Madri JA. Bone Marrow Monocyte PECAM-1 Deficiency Elicits Increased Osteoclastogenesis Resulting in Trabecular Bone Loss. The Journal Of Immunology 2009, 182: 2672-2679. PMID: 19234161, DOI: 10.4049/jimmunol.0802398.Peer-Reviewed Original ResearchMeSH KeywordsAgingAnimalsBone Marrow CellsBone ResorptionCell DifferentiationCells, CulturedDown-RegulationFemaleIntracellular Signaling Peptides and ProteinsMiceMice, KnockoutMonocytesOsteoclastsOsteogenesisPhosphorylationPlatelet Endothelial Cell Adhesion Molecule-1Protein Tyrosine Phosphatase, Non-Receptor Type 6Protein-Tyrosine KinasesSyk KinaseZAP-70 Protein-Tyrosine KinaseConceptsOsteoclast-like cellsKO miceBone marrowPECAM-1-null miceTrabecular bone lossPECAM-1Trabecular bone volumeSize of osteoclastsNF-kappaB ligandOsteoclast precursor culturesSHP-1 interactionsNumber of trabeculaeWT miceBM monocytesBone lossBone resorptionReceptor activatorBone volumeSHP-1Precursor culturesNull miceMiceLong bonesSyk kinaseFurther studies
2008
Engineering angiogenesis following spinal cord injury: a coculture of neural progenitor and endothelial cells in a degradable polymer implant leads to an increase in vessel density and formation of the blood–spinal cord barrier
Rauch MF, Hynes SR, Bertram J, Redmond A, Robinson R, Williams C, Xu H, Madri JA, Lavik EB. Engineering angiogenesis following spinal cord injury: a coculture of neural progenitor and endothelial cells in a degradable polymer implant leads to an increase in vessel density and formation of the blood–spinal cord barrier. European Journal Of Neuroscience 2008, 29: 132-145. PMID: 19120441, PMCID: PMC2764251, DOI: 10.1111/j.1460-9568.2008.06567.x.Peer-Reviewed Original ResearchMeSH KeywordsAbsorbable ImplantsAnimalsBlood VesselsBlood-Brain BarrierCells, CulturedCoculture TechniquesDisease Models, AnimalEndothelial CellsFemaleGlycolatesHydrogelsLactic AcidMicrocirculationNeovascularization, PhysiologicPolyglycolic AcidPolylactic Acid-Polyglycolic Acid CopolymerRatsRats, Sprague-DawleyRats, TransgenicSpinal CordSpinal Cord InjuriesStem Cell TransplantationTissue EngineeringTissue ScaffoldsTreatment OutcomeConceptsBlood-spinal cord barrierSpinal cord injuryCord injuryNeural progenitor cellsEndothelial cellsPositive stainingRat hemisection modelEndothelial barrier antigenFunctional vesselsRole of angiogenesisInjury epicenterSimilar coculturesSpinal cordNPC groupHemisection modelEC groupVessel densityLesion controlInjuryNeural regenerationProgenitor cellsAngiogenesisNeural progenitorsSubcutaneous modelCocultureDifferential Effects of Shear Stress and Cyclic Strain on Sp1 Phosphorylation by Protein Kinase Cζ Modulates Membrane Type 1–Matrix Metalloproteinase in Endothelial Cells
Kim JI, Cordova AC, Hirayama Y, Madri JA, Sumpio BE. Differential Effects of Shear Stress and Cyclic Strain on Sp1 Phosphorylation by Protein Kinase Cζ Modulates Membrane Type 1–Matrix Metalloproteinase in Endothelial Cells. Endothelium 2008, 15: 33-42. PMID: 18568943, PMCID: PMC2644408, DOI: 10.1080/10623320802092260.Peer-Reviewed Original ResearchConceptsSp1 phosphorylationMT1-MMP expressionPromoter sitesPKCzeta inhibitorProtein kinase CzetaAffinity of Sp1Egr-1 bindingProtein kinase CζExtracellular matrix remodelingEndothelial cell migrationSp1Cell migrationPhosphorylationMatrix remodelingProtein expressionCyclic strainExpressionMembrane typeEndothelial cellsKey roleCzetaInhibitorsCζMetalloproteinaseAffinity
2007
Loss of MMP-2 disrupts skeletal and craniofacial development and results in decreased bone mineralization, joint erosion and defects in osteoblast and osteoclast growth
Mosig RA, Dowling O, DiFeo A, Ramirez MC, Parker IC, Abe E, Diouri J, Al Aqeel AA, Wylie JD, Oblander SA, Madri J, Bianco P, Apte SS, Zaidi M, Doty SB, Majeska RJ, Schaffler MB, Martignetti JA. Loss of MMP-2 disrupts skeletal and craniofacial development and results in decreased bone mineralization, joint erosion and defects in osteoblast and osteoclast growth. Human Molecular Genetics 2007, 16: 1113-1123. PMID: 17400654, PMCID: PMC2576517, DOI: 10.1093/hmg/ddm060.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsArthritisBone and BonesBone RemodelingCalcification, PhysiologicCell ProliferationCells, CulturedCraniofacial AbnormalitiesGene DeletionHumansImmunohistochemistryJointsMatrix Metalloproteinase 2MiceMice, KnockoutOsteoblastsOsteoclastsReverse Transcriptase Polymerase Chain ReactionRNA, Small InterferingTime FactorsTomography, X-Ray ComputedConceptsMMP2-/- miceMMP-2Arthritis syndromeArticular cartilage destructionOsteoclast growthBone mineral densityDays of lifeWeeks of lifeWeeks of ageMMP-2 overexpressionJoint erosionsBone lossCartilage destructionNormal cell numbersPathophysiological mechanismsOsteoclast numberVivo physiological roleMineral densityControl littermatesAnatomical distributionBone disordersMurine modelMineralization defectMulticentric osteolysisDisease pathogenesis
2006
PECAM‐1 modulates thrombin‐induced tissue factor expression on endothelial cells
Zhang JJ, Kelm RJ, Biswas P, Kashgarian M, Madri JA. PECAM‐1 modulates thrombin‐induced tissue factor expression on endothelial cells. Journal Of Cellular Physiology 2006, 210: 527-537. PMID: 17111362, DOI: 10.1002/jcp.20908.Peer-Reviewed Original ResearchMeSH KeywordsActive Transport, Cell NucleusAnimalsApoptosisBlood CoagulationCells, CulturedDisease Models, AnimalDown-RegulationEarly Growth Response Protein 1Endothelial CellsFibrinHumansKidneyMaleMAP Kinase Signaling SystemMiceMice, Inbred C57BLMice, KnockoutOligodeoxyribonucleotides, AntisensePlatelet Endothelial Cell Adhesion Molecule-1Receptor, PAR-1Reperfusion InjuryRNA, MessengerThrombinThromboplastinThrombosisConceptsTissue factor expressionHuman umbilical vein endothelial cellsFactor expressionPECAM-1TF inductionEndothelial cellsP38 phosphorylationCell adhesion molecule-1Transient renal ischemiaThrombin receptor PAR-1PAR-1 antagonistsPertussis toxin inhibitionAdhesion molecule-1Endothelial cell adhesion molecule-1Receptor PAR-1PI3K-Akt phosphorylationGalphai/o subunitsPECAM-1 expressionRho-kinase activityUmbilical vein endothelial cellsVein endothelial cellsRenal ischemiaEgr-1 expressionFibrin depositionPlatelet functionModeling the neurovascular niche: VEGF‐ and BDNF‐mediated cross‐talk between neural stem cells and endothelial cells: An in vitro study
Li Q, Ford MC, Lavik EB, Madri JA. Modeling the neurovascular niche: VEGF‐ and BDNF‐mediated cross‐talk between neural stem cells and endothelial cells: An in vitro study. Journal Of Neuroscience Research 2006, 84: 1656-1668. PMID: 17061253, DOI: 10.1002/jnr.21087.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAnimalsAnimals, NewbornBrainBrain-Derived Neurotrophic FactorCell CommunicationCell ProliferationCells, CulturedCoculture TechniquesEndothelial CellsEnzyme-Linked Immunosorbent AssayGreen Fluorescent ProteinsMiceMice, Inbred C57BLMice, TransgenicMicroscopy, Electron, TransmissionModels, BiologicalNerve Tissue ProteinsNeuronsNitric OxidePlatelet Endothelial Cell Adhesion Molecule-1Stem CellsVascular Endothelial Growth Factor AConceptsBrain-derived neurotrophic factorBrain-derived endothelial cellsNeural stem cellsNeurovascular nicheTube formationResident neural stem cellsEndothelial cellsCell-derived soluble factorsVascular endothelial growth factorStem cellsNitric oxide scavengerEndothelial growth factorPaucity of dataExogenous NO donorNeurotrophic factorStem cell modulationVascular tube formationCell modulationENOS activationNO donorSoluble factorsGrowth factorNeuronal differentiationReciprocal modulationInductionPECAM-1 Affects GSK-3β-Mediated β-Catenin Phosphorylation and Degradation
Biswas P, Canosa S, Schoenfeld D, Schoenfeld J, Li P, Cheas LC, Zhang J, Cordova A, Sumpio B, Madri JA. PECAM-1 Affects GSK-3β-Mediated β-Catenin Phosphorylation and Degradation. American Journal Of Pathology 2006, 169: 314-324. PMID: 16816383, PMCID: PMC1698776, DOI: 10.2353/ajpath.2006.051112.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBeta CateninBlotting, WesternCapillary PermeabilityCells, CulturedEndothelial CellsFluorescent Antibody TechniqueGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHistamineHistamine AgentsHumansMiceModels, BiologicalPhosphatidylinositol 3-KinasesPhosphorylationPlatelet Endothelial Cell Adhesion Molecule-1Proto-Oncogene Proteins c-aktReceptors, HistamineSignal TransductionConceptsAdherens junctionsSerine phosphorylationSrc homology 2 domainBeta-catenin expression levelsAdherens junction componentsSerine phosphorylation levelEndothelial cellsΒ-catenin phosphorylationPECAM-1Cell biological responsesCytoplasmic domainSHP-2Proteosomal degradationGSK-3betaDynamic regulatorJunction componentsPhosphorylation levelsPhosphorylationEndothelial cell adhesion molecule-1Expression levelsGSK-3βBiological responsesEndothelial barrier permeabilityMice exhibitCell adhesion molecule-1
2005
Enhanced Susceptibility to Endotoxic Shock and Impaired STAT3 Signaling in CD31-Deficient Mice
Carrithers M, Tandon S, Canosa S, Michaud M, Graesser D, Madri JA. Enhanced Susceptibility to Endotoxic Shock and Impaired STAT3 Signaling in CD31-Deficient Mice. American Journal Of Pathology 2005, 166: 185-196. PMID: 15632011, PMCID: PMC1602311, DOI: 10.1016/s0002-9440(10)62243-2.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCells, CulturedDisease SusceptibilityDNA-Binding ProteinsEndothelium, VascularFemaleFlow CytometryGene Expression RegulationLipopolysaccharidesMiceMice, Inbred C57BLMice, KnockoutPlatelet Endothelial Cell Adhesion Molecule-1Pulmonary CirculationShock, SepticSpleenSTAT3 Transcription FactorTrans-ActivatorsTumor Necrosis Factor-alphaVanadatesConceptsCD31-deficient miceAcute phase responseSeptic shockEndothelial integritySerum tumor necrosis factor alphaTumor necrosis factor alphaEndothelial cellsCell adhesion molecule-1Necrosis factor alphaAdhesion molecule-1Endothelial cell adhesion molecule-1Wild-type controlsIL-6Endotoxic shockMCP-1Neutrophil transmigrationPhase responseMCP-5Factor alphaImmune stimuliVascular permeabilityInterferon gammaKnockout miceMolecule-1STAT3 Signaling
2004
Noninvasive imaging of myocardial angiogenesis following experimental myocardial infarction
Meoli DF, Sadeghi MM, Krassilnikova S, Bourke BN, Giordano FJ, Dione DP, Su H, Edwards DS, Liu S, Harris TD, Madri JA, Zaret BL, Sinusas AJ. Noninvasive imaging of myocardial angiogenesis following experimental myocardial infarction. Journal Of Clinical Investigation 2004, 113: 1684-1691. PMID: 15199403, PMCID: PMC420502, DOI: 10.1172/jci20352.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCells, CulturedCoronary VesselsDiagnostic ImagingDogsEndothelial CellsEndothelium, VascularHemodynamicsIndium RadioisotopesIntegrin alphaVbeta3MaleMolecular StructureMyocardial InfarctionMyocardiumNeovascularization, PhysiologicQuinolonesRadiopharmaceuticalsRatsRats, Sprague-DawleyTechnetium Tc 99m SestamibiTomography, Emission-Computed, Single-PhotonConceptsMyocardial angiogenesisMyocardial infarctionRadiotracer uptakeInjury-induced angiogenesisChronic rat modelNoninvasive imaging strategiesTherapeutic myocardial angiogenesisExperimental myocardial infarctionFocal radiotracer uptakePotential novel targetSignificant clinical utilityAlphavbeta3 integrinRisk stratificationHistological evidenceHypoperfused regionsRat modelMyocardial radiotracer uptakeClinical utilityNoninvasive evaluationAngiogenic therapyCanine modelInfarct regionInfarctionNovel targetNoninvasive imaging
2003
Transcriptional Up-regulation of Endothelial Cell Matrix Metalloproteinase-2 in Response to Extracellular Cues Involves GATA-2*
Han X, Boyd PJ, Colgan S, Madri JA, Haas TL. Transcriptional Up-regulation of Endothelial Cell Matrix Metalloproteinase-2 in Response to Extracellular Cues Involves GATA-2*. Journal Of Biological Chemistry 2003, 278: 47785-47791. PMID: 14512418, DOI: 10.1074/jbc.m309482200.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBase SequenceBlotting, NorthernBlotting, WesternCell NucleusCells, CulturedCollagenCOS CellsDNA-Binding ProteinsEndothelial CellsExtracellular MatrixGATA2 Transcription FactorGelatinGenes, ReporterLuciferasesMatrix Metalloproteinase 2MicrocirculationMolecular Sequence DataNeovascularization, PhysiologicPhenotypePromoter Regions, GeneticProtein BindingRatsTranscription FactorsTranscription, GeneticTranscriptional ActivationTransfectionUp-Regulation