2015
Modulation of Sox10, HIF-1α, Survivin, and YAP by Minocycline in the Treatment of Neurodevelopmental Handicaps following Hypoxic Insult
Li Q, Tsuneki M, Krauthammer M, Couture R, Schwartz M, Madri JA. Modulation of Sox10, HIF-1α, Survivin, and YAP by Minocycline in the Treatment of Neurodevelopmental Handicaps following Hypoxic Insult. American Journal Of Pathology 2015, 185: 2364-2378. PMID: 26209807, PMCID: PMC5801488, DOI: 10.1016/j.ajpath.2015.05.016.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsApoptosisCell Cycle ProteinsDisease Models, AnimalHypoxiaHypoxia-Inducible Factor 1, alpha SubunitInhibitor of Apoptosis ProteinsMice, Inbred C57BLMinocyclineMultiple SclerosisPhosphoproteinsRepressor ProteinsSOXE Transcription FactorsSurvivinUp-RegulationYAP-Signaling ProteinsConceptsMinocycline treatmentNeurodevelopmental handicapHypoxic insultEffects of minocyclineUntoward side effectsAnimal model studiesPotential therapeutic targetSublethal hypoxic conditionsPremature infantsMultiple sclerosisCurrent therapiesTreatment trialsChronic hypoxiaSynaptic transmissionMurine modelMouse pupsMotor handicapNewborn populationSide effectsTherapeutic targetSublethal hypoxiaHIF-1αNerve transmissionMinocyclineCognitive function
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
Modeling the neurovascular niche: implications for recovery from CNS injury.
Madri JA. Modeling the neurovascular niche: implications for recovery from CNS injury. Journal Of Physiology And Pharmacology 2009, 60 Suppl 4: 95-104. PMID: 20083857.Peer-Reviewed Original ResearchConceptsNeurovascular nicheCNS injuryHIF-1alphaSpinal cord injuryNeural stem cell survivalNeurogenic zonesCord injuryTraumatic brainMurine modelSDF-1Sublethal hypoxiaInjuryStem cell survivalNRP-1Neurodegenerative diseasesEndothelial cellsHypoxiaExpression levelsSurvivalCell survivalFocused reviewDiseaseVariable responseTrkBBDNF
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
1997
Involvement of endothelial PECAM-1/CD31 in angiogenesis.
DeLisser H, Christofidou-Solomidou M, Strieter R, Burdick M, Robinson C, Wexler R, Kerr J, Garlanda C, Merwin J, Madri J, Albelda S. Involvement of endothelial PECAM-1/CD31 in angiogenesis. American Journal Of Pathology 1997, 151: 671-7. PMID: 9284815, PMCID: PMC1857836.Peer-Reviewed Original ResearchMeSH KeywordsAngiotensin-Converting Enzyme InhibitorsAnimalsAntibodies, MonoclonalCells, CulturedCollagenCorneaDrug CombinationsEndotheliumFibroblast Growth Factor 2HumansLamininMiceMice, Inbred C57BLNeovascularization, PhysiologicPlatelet Endothelial Cell Adhesion Molecule-1ProteoglycansRatsRats, Sprague-DawleyTransforming Growth Factor betaConceptsCell-cell adhesion moleculesEndothelial cell-cell adhesion moleculesBasic fibroblast growth factorRat capillary endothelial cellsPECAM-1Adhesion moleculesHuman PECAM-1Murine PECAM-1Endothelial cellsFibroblast growth factorAdhesion receptorsProcess of angiogenesisPECAM-1/CD31Tube formationAdhesive interactionsVessel growthGrowth factorCapillary endothelial cellsPolyclonal antibodiesRat corneal neovascularizationAngiogenesisCorneal neovascularizationCellsMurine modelMonoclonal antibodies