2009
Proteomic-Based Detection of a Protein Cluster Dysregulated during Cardiovascular Development Identifies Biomarkers of Congenital Heart Defects
Nath AK, Krauthammer M, Li P, Davidov E, Butler LC, Copel J, Katajamaa M, Oresic M, Buhimschi I, Buhimschi C, Snyder M, Madri JA. Proteomic-Based Detection of a Protein Cluster Dysregulated during Cardiovascular Development Identifies Biomarkers of Congenital Heart Defects. PLOS ONE 2009, 4: e4221. PMID: 19156209, PMCID: PMC2626248, DOI: 10.1371/journal.pone.0004221.Peer-Reviewed Original ResearchConceptsCardiovascular developmentMass spectrometry-based proteomicsSpectrometry-based proteomicsNormal cardiovascular developmentAdhesion/migrationHuman CHDsProteomic datasetsHeart developmentProtein clustersMurine embryosProtein pathwayMolecular pathwaysFunctional roleProteinEmbryonic survivalYolk sacProtein levelsIdentifies biomarkersCardiovascular defectsWestern blottingPathwayNovel avenuesEmbryosComplete understandingProtein biomarkers
2007
Modeling the neurovascular niche: Murine strain differences mimic the range of responses to chronic hypoxia in the premature newborn
Li Q, Michaud M, Stewart W, Schwartz M, Madri JA. Modeling the neurovascular niche: Murine strain differences mimic the range of responses to chronic hypoxia in the premature newborn. Journal Of Neuroscience Research 2007, 86: 1227-1242. PMID: 18092360, PMCID: PMC2644407, DOI: 10.1002/jnr.21597.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornApoptosisBlotting, WesternBrainCell ProliferationDisease Models, AnimalGene ExpressionHematopoiesis, ExtramedullaryHumansHypoxia, BrainImmunohistochemistryImmunoprecipitationInfant, NewbornInfant, PrematureIntercellular Signaling Peptides and ProteinsMiceMice, Inbred C57BLNitric OxideStem CellsConceptsNeural progenitor cellsChronic hypoxiaSubventricular zonePreterm birth resultsLow baseline levelsHypoxia-induced levelsNeurogenic responseNeurovascular nicheHypoxic insultBlunted responseBirth resultsC57BL/6 pupsBaseline levelsMotor disabilityMouse strainsGrowth factorVariable recoveryHypoxiaProgenitor cellsPupsRecent evidenceSignificant cognitiveHypoxicApoptotic responseResponse
2006
Modeling 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 modulationInductionThe roles of nitric oxide in murine cardiovascular development
Nath AK, Madri JA. The roles of nitric oxide in murine cardiovascular development. Developmental Biology 2006, 292: 25-33. PMID: 16442519, DOI: 10.1016/j.ydbio.2005.12.039.Peer-Reviewed Original ResearchConceptsMammalian organ systemsCardiovascular developmentCell contextBiological functionsOrgan system developmentRedox milieuRegulatory roleDiverse arrayRole of NOBiochemical environmentOrgan systemsNitric oxidePathological statesParadoxical actionPotential implicationsRoleReproductionProduction of NOSystem developmentCytoprotectionWide range
2004
Nitric oxide modulates murine yolk sac vasculogenesis and rescues glucose induced vasculopathy
Nath AK, Enciso J, Kuniyasu M, Hao XY, Madri JA, Pinter E. Nitric oxide modulates murine yolk sac vasculogenesis and rescues glucose induced vasculopathy. Development 2004, 131: 2485-2496. PMID: 15128676, DOI: 10.1242/dev.01131.Peer-Reviewed Original ResearchConceptsVascular developmentReactive oxygen speciesYolk sac vasculogenesisMurine yolk sacYolk sacBlood island formationEnvironmental insultsNormal embryonic growthMurine embryo culturePreimplantation embryogenesisAbnormal vascular developmentGenetic manipulationDevelopmental arrestExpression patternsPostimplantation developmentNitric oxideEndodermal layerEmbryonic growthFunctional inactivationHigh glucoseROS productionRole of NOBlastocyst invasionProtein levelsEmbryo cultureHistamine 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
2003
Abolition of arteriolar dilation but not constriction to histamine in cremaster muscle of eNOS–/– mice
Payne GW, Madri JA, Sessa WC, Segal SS. Abolition of arteriolar dilation but not constriction to histamine in cremaster muscle of eNOS–/– mice. AJP Heart And Circulatory Physiology 2003, 285: h493-h498. PMID: 12689855, DOI: 10.1152/ajpheart.00071.2003.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsArteriolesCimetidineEndothelium, VascularHistamineHistamine H1 AntagonistsHistamine H2 AntagonistsMaleMiceMice, Inbred C57BLMice, Inbred StrainsMuscle, SkeletalNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIPlatelet Endothelial Cell Adhesion Molecule-1PyrilamineReceptors, HistamineSignal TransductionVasoconstrictionVasodilationConceptsENOS-/- miceMuscle blood flowVasomotor responsesBlood flowCremaster muscleCell adhesion molecule-1Anesthetized C57Bl6 miceBiphasic vasomotor responseSecond-order arteriolesAdhesion molecule-1Endothelial cell adhesion molecule-1Platelet endothelial cell adhesion molecule-1Nitric oxide releaseTopical histamineConstrictor responsesArteriolar dilationNomega-nitroC57BL6 miceH1 receptorsPharmacological interventionsPermeability of capillariesSmooth muscleMicrovascular endotheliumTissue perfusionCumulative addition
1997
Nitric oxide production contributes to the angiogenic properties of vascular endothelial growth factor in human endothelial cells.
Papapetropoulos A, García-Cardeña G, Madri JA, Sessa WC. Nitric oxide production contributes to the angiogenic properties of vascular endothelial growth factor in human endothelial cells. Journal Of Clinical Investigation 1997, 100: 3131-3139. PMID: 9399960, PMCID: PMC508526, DOI: 10.1172/jci119868.Peer-Reviewed Original ResearchConceptsHuman umbilical vein endothelial cellsVascular endothelial growth factorPhosphoinositide-3 kinase inhibitorDimensional collagen gelsRegulator of vasculogenesisKinase inhibitorsGrowth of HUVECsGrowth factorExposure of cellsUmbilical vein endothelial cellsEndothelial cellsTyrosine kinaseHuman endothelial cellsVEGF stimulationSynthase proteinK kinaseEndothelial growth factorVein endothelial cellsProtein levelsEC proliferationKinaseHuman ECsDependent formationNO-dependent mannerShort-term stimulationNitric oxide synthase inhibitors attenuate transforming-growth-factor-beta 1-stimulated capillary organization in vitro.
Papapetropoulos A, Desai KM, Rudic RD, Mayer B, Zhang R, Ruiz-Torres MP, García-Cardeña G, Madri JA, Sessa WC. Nitric oxide synthase inhibitors attenuate transforming-growth-factor-beta 1-stimulated capillary organization in vitro. American Journal Of Pathology 1997, 150: 1835-44. PMID: 9137106, PMCID: PMC1858220.Peer-Reviewed Original ResearchConceptsNitric oxideL-NAMETube formationNOS isoformsNitric oxide synthase inhibitorL-nitro-arginine methylesterOxide synthase inhibitorNO donor sodium nitroprussideRole of NOTranscriptase-polymerase chain reactionExcess L-arginineDonor sodium nitroprussideSoluble guanylate cyclaseWestern blot analysisEndothelial cell proliferationNOS blockadeCapillary tube formationEndothelial NOSSodium nitroprussideSynthase inhibitorL-arginineMicrovascular ECsAutocrine productionGuanylate cyclaseCapillary organization