2017
CD44 Promotes Inflammation and Extracellular Matrix Production During Arteriovenous Fistula Maturation
Kuwahara G, Hashimoto T, Tsuneki M, Yamamoto K, Assi R, Foster TR, Hanisch JJ, Bai H, Hu H, Protack CD, Hall MR, Schardt JS, Jay SM, Madri JA, Kodama S, Dardik A. CD44 Promotes Inflammation and Extracellular Matrix Production During Arteriovenous Fistula Maturation. Arteriosclerosis Thrombosis And Vascular Biology 2017, 37: 1147-1156. PMID: 28450292, PMCID: PMC5467640, DOI: 10.1161/atvbaha.117.309385.Peer-Reviewed Original ResearchConceptsExtracellular matrix depositionKnockout miceExtracellular matrix componentsExtracellular matrix productionMatrix depositionAdhesion molecule-1 expressionM2 macrophagesProtein 1Matrix productionCell adhesion molecule-1 expressionMolecule-1 expressionProtein expressionMatrix componentsCD44 knockout miceProtein-1 expressionMajor receptorCD44 activityMaturationVascular cell adhesion molecule-1 expressionAdhesion moleculesExpressionCD44 mRNAChemoattractant protein-1 expressionWild-type C57BL/6JArteriovenous fistulaNOD Mice Having a Lyn Tyrosine Kinase Mutation Exhibit Abnormal Neutrophil Chemotaxis
Wu Y, Hannigan M, Zhan L, Madri JA, Huang C. NOD Mice Having a Lyn Tyrosine Kinase Mutation Exhibit Abnormal Neutrophil Chemotaxis. Journal Of Cellular Physiology 2017, 232: 1689-1695. PMID: 27591397, DOI: 10.1002/jcp.25583.Peer-Reviewed Original ResearchIncreased Oxidative Stress and Hypoxia Inducible Factor-1 Expression during Arteriovenous Fistula Maturation
Sadaghianloo N, Yamamoto K, Bai H, Tsuneki M, Protack CD, Hall MR, Declemy S, Hassen-Khodja R, Madri J, Dardik A. Increased Oxidative Stress and Hypoxia Inducible Factor-1 Expression during Arteriovenous Fistula Maturation. Annals Of Vascular Surgery 2017, 41: 225-234. PMID: 28163173, PMCID: PMC5411319, DOI: 10.1016/j.avsg.2016.09.014.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAortaArteriovenous Shunt, SurgicalGene Expression RegulationHeme Oxygenase-1Hydrogen PeroxideHyperplasiaHypoxia-Inducible Factor 1, alpha SubunitMaleMembrane ProteinsMice, Inbred C57BLNADPH Oxidase 2NeointimaOxidative StressReactive Oxygen SpeciesSignal TransductionTime FactorsTyrosineVascular Endothelial Growth Factor AVascular PatencyVena Cava, InferiorConceptsHeme oxygenase-1Arteriovenous fistulaAVF maturationNOX-2HIF-1αOxidative stressHypoxia-inducible factor 1 (HIF-1) expressionSham-operated micePoor clinical resultsHIF-1α immunoreactivityInferior vena cavaArteriovenous fistula maturationVascular endothelial growth factorHypoxia-inducible factor-1 (HIF-1) pathwayFactor-1 expressionEndothelial growth factorHIF-1 pathwayHuman AVF maturationQuantitative polymerase chain reactionOxidative stress increasesAortocaval fistulaFistula maturationVena cavaClinical resultsPolymerase chain reactionThe 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
2016
Targeted proteomics effectively quantifies differences between native lung and detergent-decellularized lung extracellular matrices
Calle EA, Hill RC, Leiby KL, Le AV, Gard AL, Madri JA, Hansen KC, Niklason LE. Targeted proteomics effectively quantifies differences between native lung and detergent-decellularized lung extracellular matrices. Acta Biomaterialia 2016, 46: 91-100. PMID: 27693690, PMCID: PMC5451113, DOI: 10.1016/j.actbio.2016.09.043.Peer-Reviewed Original ResearchConceptsExtracellular matrixLung extracellular matrixMatrix proteinsECM-associated proteinsCell-matrix interactionsProtein extraction methodsWhole organ regenerationRegenerative medicineOrganotypic cell culturesQuantitative proteomicsAcellular extracellular matrixECM proteinsOrgan regenerationCell adhesionProteomicsProtein analysisQuantitative biochemical dataProteinPotent substrateXenogeneic extracellular matrixTargeted proteomicsCell nuclear antigenBiochemical dataImportant glycoproteinCell cultures
2015
ENPP1-Fc prevents mortality and vascular calcifications in rodent model of generalized arterial calcification of infancy
Albright RA, Stabach P, Cao W, Kavanagh D, Mullen I, Braddock AA, Covo MS, Tehan M, Yang G, Cheng Z, Bouchard K, Yu ZX, Thorn S, Wang X, Folta-Stogniew EJ, Negrete A, Sinusas AJ, Shiloach J, Zubal G, Madri JA, De La Cruz EM, Braddock DT. ENPP1-Fc prevents mortality and vascular calcifications in rodent model of generalized arterial calcification of infancy. Nature Communications 2015, 6: 10006. PMID: 26624227, PMCID: PMC4686714, DOI: 10.1038/ncomms10006.Peer-Reviewed Original ResearchConceptsChronic kidney diseaseVascular calcificationArterial calcificationOrphan diseaseCommon diseaseSequelae of diseaseEctopic vascular calcificationInternal elastic laminaPrevent mortalityRenal failureCardiac failureKidney diseaseSubcutaneous administrationRodent modelsAnimal modelsEctopic calcificationVascular wallLarge arteriesElastic laminaDiseaseCalcificationCalciphylaxisDecreased concentrationSclerosisArteryA 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
Temporal Regulation of venous Extracellular Matrix Components during Arteriovenous Fistula Maturation
Hall MR, Yamamoto K, Protack CD, Tsuneki M, Kuwahara G, Assi R, Brownson KE, Bai H, Madri JA, Dardik A. Temporal Regulation of venous Extracellular Matrix Components during Arteriovenous Fistula Maturation. The Journal Of Vascular Access 2014, 16: 93-106. PMID: 25262757, PMCID: PMC4405006, DOI: 10.5301/jva.5000290.Peer-Reviewed Original ResearchConceptsExtracellular matrix componentsTemporal regulationECM componentsStructural proteinsMatrix componentsGene microarray analysisMatrix metalloproteinasesRegulatory proteinsMicroarray analysisNon-collagenous proteinsDistinct temporal patternsECM degradationTemporal patternsProteinProtein expressionElastin expressionExpressionMaturationOsteopontin expressionProtease inhibitorsHuman AVF maturationRegulationTissue inhibitorDays of maturationMetalloproteinase-1
2011
Brain regional angiogenic potential at the neurovascular unit during normal aging
Murugesan N, Demarest TG, Madri JA, Pachter JS. Brain regional angiogenic potential at the neurovascular unit during normal aging. Neurobiology Of Aging 2011, 33: 1004.e1-1004.e16. PMID: 22019053, PMCID: PMC3266473, DOI: 10.1016/j.neurobiolaging.2011.09.022.Peer-Reviewed Original ResearchConceptsNeurovascular unitPhysical exerciseNormal agingPolymerase chain reactionAngiogenesis-associated genesDiscrete brain regionsRegion-dependent wayReal-time polymerase chain reactionWeak angiogenic responseRegion-dependent mannerQuantitative real-time polymerase chain reactionCerebral angiogenesisAged brainAged miceLaser capture microdissectionTherapeutic benefitAge-related trendsBrain regionsAngiogenic capacityAngiogenic responseAngiogenic potentialChain reactionCapture microdissectionBrainHypoxiaCharacterization of the Natural History of Extracellular Matrix Production in Tissue-Engineered Vascular Grafts during Neovessel Formation
Naito Y, Williams-Fritze M, Duncan DR, Church SN, Hibino N, Madri JA, Humphrey JD, Shinoka T, Breuer CK. Characterization of the Natural History of Extracellular Matrix Production in Tissue-Engineered Vascular Grafts during Neovessel Formation. Cells Tissues Organs 2011, 195: 60-72. PMID: 21996715, PMCID: PMC3257815, DOI: 10.1159/000331405.Peer-Reviewed Original ResearchGSK-3β: a signaling pathway node modulating neural stem cell and endothelial cell interactions
Li Q, Michaud M, Canosa S, Kuo A, Madri JA. GSK-3β: a signaling pathway node modulating neural stem cell and endothelial cell interactions. Angiogenesis 2011, 14: 173-185. PMID: 21253820, DOI: 10.1007/s10456-011-9201-9.Peer-Reviewed Original ResearchMeSH KeywordsAminophenolsAnimalsBasic Helix-Loop-Helix Transcription FactorsBeta CateninBrainCell CommunicationCell DifferentiationCell MovementCell ProliferationEndothelial CellsEnzyme ActivationGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHypoxia-Inducible Factor 1, alpha SubunitIntercellular Signaling Peptides and ProteinsMaleMaleimidesMiceMice, Inbred C57BLNeovascularization, PhysiologicNeural Stem CellsNeurogenesisPhosphorylationPhosphoserineReceptor Cross-TalkSignal TransductionSolubilitySpecies SpecificityConceptsNeural stem cellsNotch-1 expressionHIF-1αGSK-3βSDF-1III-tubulinStem cellsPremature infant populationMicrovascular endothelial cellsGSK-3β activationCD1 levelsEndothelial cell interactionsNeurogenic areasVascular proliferationInfant populationGSK-3β inhibitorTherapeutic potentialSVZ tissueGreater angiogenesisHIF-2αMouse strainsΒ-catenin participatesEndothelial cellsReciprocal modulation
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 survival
2008
Targeted imaging of hypoxia-induced integrin activation in myocardium early after infarction
Kalinowski L, Dobrucki LW, Meoli DF, Dione DP, Sadeghi MM, Madri JA, Sinusas AJ. Targeted imaging of hypoxia-induced integrin activation in myocardium early after infarction. Journal Of Applied Physiology 2008, 104: 1504-1512. PMID: 18356482, DOI: 10.1152/japplphysiol.00861.2007.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsBiomarkersBiotransformationDogsHeterocyclic Compounds, 1-RingHypoxiaImidazolesImmunohistochemistryIntegrin alphaVbeta3IntegrinsMaleMyocardial InfarctionMyocardial IschemiaMyocardiumNeovascularization, PhysiologicOrganometallic CompoundsOrganotechnetium CompoundsRadiopharmaceuticalsRatsRats, Sprague-DawleyTechnetium Tc 99m SestamibiTomography, Emission-Computed, Single-PhotonConceptsMyocardial infarctionInfarct regionCanine studyIschemic heart diseaseCoronary artery occlusionAcute myocardial infarctionMarkers of angiogenesisEx vivo analysisExpression/activationPotential novel targetHypoxia-induced angiogenesisVivo SPECT imagingAlphavbeta3 integrinBRU59-21Artery occlusionNovel noninvasive approachHeart diseaseHistological evidenceMyocardial hypoxiaMyocardial uptakeRP748Rodent studiesAngiogenic therapyInfarctionMyocardial angiogenesisDifferential 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
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 functionEffects of a novel tylophorine analog on collagen‐induced arthritis through inhibition of the innate immune response
You X, Pan M, Gao W, Shiah H, Tao J, Zhang D, Koumpouras F, Wang S, Zhao H, Madri JA, Baker D, Cheng Y, Yin Z. Effects of a novel tylophorine analog on collagen‐induced arthritis through inhibition of the innate immune response. Arthritis & Rheumatism 2006, 54: 877-886. PMID: 16508970, DOI: 10.1002/art.21640.Peer-Reviewed Original ResearchConceptsCollagen-induced arthritisBone marrow-derived dendritic cellsMarrow-derived dendritic cellsInnate immune responseDendritic cellsProinflammatory cytokinesTylophorine analogsImmune responseOnset of CIAProgression of CIACytometric bead array analysisTumor necrosis factor alphaB cell antibody responseDevelopment of arthritisNecrosis factor alphaT cell proliferationBead array analysisNovel therapeutic agentsEnzyme-linked immunosorbent assayInflammatory arthritisJoint inflammationInflammatory cytokinesAntibody responseClinical severityPathologic changes
2005
Noninvasive Imaging of Angiogenesis With a 99mTc-Labeled Peptide Targeted at αvβ3 Integrin After Murine Hindlimb Ischemia
Hua J, Dobrucki LW, Sadeghi MM, Zhang J, Bourke BN, Cavaliere P, Song J, Chow C, Jahanshad N, van Royen N, Buschmann I, Madri JA, Mendizabal M, Sinusas AJ. Noninvasive Imaging of Angiogenesis With a 99mTc-Labeled Peptide Targeted at αvβ3 Integrin After Murine Hindlimb Ischemia. Circulation 2005, 111: 3255-3260. PMID: 15956134, DOI: 10.1161/circulationaha.104.485029.Peer-Reviewed Original ResearchRole of C5 in the development of airway inflammation, airway hyperresponsiveness, and ongoing airway response
Peng T, Hao L, Madri JA, Su X, Elias JA, Stahl GL, Squinto S, Wang Y. Role of C5 in the development of airway inflammation, airway hyperresponsiveness, and ongoing airway response. Journal Of Clinical Investigation 2005, 115: 1590-1600. PMID: 15902311, PMCID: PMC1090470, DOI: 10.1172/jci22906.Peer-Reviewed Original ResearchConceptsAirway hyperresponsivenessAirway inflammationContribution of C5Airway responsesDevelopment of AHRHarmful inflammatory mediatorsRole of C5C5-deficient miceCourse of diseaseDownstream inflammatory cascadesInnate immune systemPotential clinical approachCritical checkpointAllergen provocationComplement component C5Inflammatory mediatorsInflammatory cascadeAirway lumenInflammatory cellsC5 inhibitionNonspecific stimuliClinical approachImmune systemInflammationC5b-9
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 imagingHistamine inhibits conducted vasodilation through endothelium‐derived NO production in arterioles of mouse skeletal muscle
Payne GW, Madri JA, Sessa WC, Segal SS. Histamine inhibits conducted vasodilation through endothelium‐derived NO production in arterioles of mouse skeletal muscle. The FASEB Journal 2004, 18: 280-286. PMID: 14769822, DOI: 10.1096/fj.03-0752com.Peer-Reviewed Original ResearchMeSH KeywordsAcetylcholineAnimalsArteriolesEndothelium, VascularFemaleGene DeletionGuanylate CyclaseHistamineMaleMiceMice, Inbred C57BLMice, KnockoutMuscle, SkeletalNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIPlatelet Endothelial Cell Adhesion Molecule-1VasodilationConceptsENOS-/- miceArteriolar endotheliumEndothelium-derived NO productionSpread of hyperpolarizationNO-dependent mechanismSecond-order arteriolesIntercellular adhesion moleculeGap junction channelsSoluble guanylate cyclaseAcetylcholine microiontophoresisHistamine inhibitsLocal vasodilationMouse skeletal muscleNO synthaseVenular endotheliumVasodilationCremaster muscleMaximal diameterNO productionArteriolesHistamineJunction channelsGuanylate cyclaseEndotheliumAdhesion molecules