2017
The 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
2011
A critical role for macrophages in neovessel formation and the development of stenosis in tissue‐engineered vascular grafts
Hibino N, Yi T, Duncan DR, Rathore A, Dean E, Naito Y, Dardik A, Kyriakides T, Madri J, Pober JS, Shinoka T, Breuer CK. A critical role for macrophages in neovessel formation and the development of stenosis in tissue‐engineered vascular grafts. The FASEB Journal 2011, 25: 4253-4263. PMID: 21865316, PMCID: PMC3236622, DOI: 10.1096/fj.11-186585.Peer-Reviewed Original ResearchConceptsMacrophage infiltrationNeovessel formationGraft-related complicationsIncidence of stenosisTissue-engineered vascular graftsDevelopment of stenosisTransgenic mouse modelRole of macrophagesFirst clinical trialSmooth muscle cellsVascular graftsTEVG stenosisMacrophage infiltratesClodronate liposomesClinical trialsM1 macrophagesM2 phenotypeMurine modelMouse modelStenosisSeeded graftsRole of cellNatural historyMuscle cellsMacrophages
2009
VEGF-A and Semaphorin3A: Modulators of vascular sympathetic innervation
Long JB, Jay SM, Segal SS, Madri JA. VEGF-A and Semaphorin3A: Modulators of vascular sympathetic innervation. Developmental Biology 2009, 334: 119-132. PMID: 19631637, PMCID: PMC2871302, DOI: 10.1016/j.ydbio.2009.07.023.Peer-Reviewed Original Research
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 modulationInduction
2001
PECAM-1 Is a Modulator of STAT Family Member Phosphorylation and Localization: Lessons from a Transgenic Mouse
Ilan N, Cheung L, Miller S, Mohsenin A, Tucker A, Madri J. PECAM-1 Is a Modulator of STAT Family Member Phosphorylation and Localization: Lessons from a Transgenic Mouse. Developmental Biology 2001, 232: 219-232. PMID: 11254359, DOI: 10.1006/dbio.2001.0186.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell DivisionCell NucleusCells, CulturedDNA-Binding ProteinsEndothelium, VascularFemaleHumansMammary Glands, AnimalMiceMice, TransgenicMilk ProteinsMorphogenesisPhosphorylationPlatelet Endothelial Cell Adhesion Molecule-1Pulmonary AlveoliSTAT5 Transcription FactorTrans-ActivatorsTumor Suppressor ProteinsConceptsImmunoreceptor tyrosine activation motifMilk protein gene expressionPhosphorylation levelsSignal transduction pathwaysProtein gene expressionTyrosine activation motifTyrosine phosphorylation levelsPECAM-1Cell cycle progressionMammary gland developmentInduction of p21Cytoplasmic tailBranching morphogenesisTransduction pathwaysTransgenic miceActivation motifCell adhesion moleculeDuctal epithelial cell proliferationGene expressionCycle progressionGland developmentEpithelial cell proliferationDuctal branching morphogenesisCell proliferationVascular cells
2000
Distinct roles for matrix metalloproteinase-2 and α4 integrin in autoimmune T cell extravasation and residency in brain parenchyma during experimental autoimmune encephalomyelitis
Graesser D, Mahooti S, Madri J. Distinct roles for matrix metalloproteinase-2 and α4 integrin in autoimmune T cell extravasation and residency in brain parenchyma during experimental autoimmune encephalomyelitis. Journal Of Neuroimmunology 2000, 109: 121-131. PMID: 10996214, DOI: 10.1016/s0165-5728(00)00275-7.Peer-Reviewed Original ResearchConceptsMatrix metalloproteinase-2Auto-reactive T cellsExpression of alpha4T cellsMetalloproteinase-2Human multiple sclerosisExperimental autoimmune encephalomyelitisT cell extravasationMMP-2 inductionCentral nervous systemAutoimmune encephalomyelitisMultiple sclerosisAutoimmune diseasesBrain parenchymaNervous systemΑ4 integrinAlpha4 integrinsCell extravasationIndependent roleEAEAlpha4Basement membrane matrixInductionDistinct rolesIntegrins