2023
Transendothelial Migration of Human B Cells: Chemokine versus Antigen.
Wang V, Pober J, Manes T. Transendothelial Migration of Human B Cells: Chemokine versus Antigen. The Journal Of Immunology 2023, 211: 923-931. PMID: 37530585, PMCID: PMC10529164, DOI: 10.4049/jimmunol.2200887.Peer-Reviewed Original ResearchConceptsB cellsLeukocyte cell adhesion moleculeTransendothelial migrationEndothelial cellsCell adhesion moleculeAdhesion moleculesPeripheral blood CD19B cell subsetsMemory B cellsInnate immune propertiesSites of inflammationMicrovascular endothelial cellsHuman microvascular endothelial cellsHuman B cellsBlood CD19Peripheral bloodCell subsetsVenular flowT cellsICAM-1VCAM-1Immune propertiesSyk activationChemokinesExpression of genes
2020
Mural Cell-Specific Deletion of Cerebral Cavernous Malformation 3 in the Brain Induces Cerebral Cavernous Malformations
Wang K, Zhang H, He Y, Jiang Q, Tanaka Y, Park IH, Pober JS, Min W, Zhou HJ. Mural Cell-Specific Deletion of Cerebral Cavernous Malformation 3 in the Brain Induces Cerebral Cavernous Malformations. Arteriosclerosis Thrombosis And Vascular Biology 2020, 40: 2171-2186. PMID: 32640906, DOI: 10.1161/atvbaha.120.314586.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosis Regulatory ProteinsBrainCell CommunicationCell MovementCells, CulturedCoculture TechniquesEndothelial CellsFemaleFocal AdhesionsGene DeletionGenetic Predisposition to DiseaseHemangioma, Cavernous, Central Nervous SystemHumansMaleMembrane ProteinsMice, KnockoutMicrovesselsMyocytes, Smooth MusclePaxillinPericytesPhenotypeProtein StabilityProto-Oncogene ProteinsSignal TransductionConceptsCerebral cavernous malformationsBrain mural cellsCCM lesionsMural cellsCavernous malformationsSevere brain hemorrhageCCM pathogenesisSmooth muscle cellsWeeks of ageCell-specific deletionMural cell coverageBrain pericytesBrain hemorrhageNeonatal stageBrain vasculatureLesionsEntire brainMuscle cellsCerebral cavernous malformation 3Endothelial cellsMicePericytesSpecific deletionAdhesion formationPathogenesis
2019
Three Dimensional Bioprinting of a Vascularized and Perfusable Skin Graft Using Human Keratinocytes, Fibroblasts, Pericytes, and Endothelial Cells
Baltazar T, Merola J, Catarino C, Xie C, Kirkiles-Smith N, Lee V, Hotta S, Dai G, Xu X, Ferreira FC, Saltzman WM, Pober JS, Karande P. Three Dimensional Bioprinting of a Vascularized and Perfusable Skin Graft Using Human Keratinocytes, Fibroblasts, Pericytes, and Endothelial Cells. Tissue Engineering Part A 2019, 26: 227-238. PMID: 31672103, PMCID: PMC7476394, DOI: 10.1089/ten.tea.2019.0201.Peer-Reviewed Original ResearchConceptsSkin graftsHuman endothelial colony-forming cellsEndothelial cellsHuman endothelial cellsHuman skin graftsEndothelial colony-forming cellsPlacental pericytesGraft survivalCutaneous ulcersAllogeneic cellsHuman foreskin keratinocytesMouse microvesselsImmunodeficient miceHuman pericytesGraftColony-forming cellsVascular structuresWound bedForeskin keratinocytesEpidermal maturationPericytesHuman placental pericytesHuman keratinocytesKeratinocytesType I
2016
Complement C5 Inhibition Reduces T Cell–Mediated Allograft Vasculopathy Caused by Both Alloantibody and Ischemia Reperfusion Injury in Humanized Mice
Qin L, Li G, Kirkiles‐Smith N, Clark P, Fang C, Wang Y, Yu Z, Devore D, Tellides G, Pober J, Jane‐Wit D. Complement C5 Inhibition Reduces T Cell–Mediated Allograft Vasculopathy Caused by Both Alloantibody and Ischemia Reperfusion Injury in Humanized Mice. American Journal Of Transplantation 2016, 16: 2865-2876. PMID: 27104811, PMCID: PMC5075274, DOI: 10.1111/ajt.13834.Peer-Reviewed Original ResearchConceptsIschemia-reperfusion injuryAllograft vasculopathyEndothelial cell activationReperfusion injuryCell activationComplement C5 inhibitionNuclear factor kappa BSolid organ transplantsT cell infiltrationTerminal complement activationVCAM-1 expressionComplement C5 activationFactor kappa BNeutrophil infiltrationHumanized miceDiffuse stenosisIntraluminal thrombosisArterial graftsC5 inhibitionCell infiltrationHumanized modelNeointimal hyperplasiaOrgan transplantsAlloantibodiesNF-kB
2015
Tissue-Engineered Microvasculature to Reperfuse Isolated Renal Glomeruli
Chang WG, Fornoni A, Tietjen G, Mendez JJ, Niklason LE, Saltzman WM, Pober JS. Tissue-Engineered Microvasculature to Reperfuse Isolated Renal Glomeruli. Tissue Engineering Part A 2015, 21: 2673-2679. PMID: 26414101, PMCID: PMC4652181, DOI: 10.1089/ten.tea.2015.0060.Peer-Reviewed Original ResearchEfficient Gene Disruption in Cultured Primary Human Endothelial Cells by CRISPR/Cas9
Abrahimi P, Chang WG, Kluger MS, Qyang Y, Tellides G, Saltzman WM, Pober JS. Efficient Gene Disruption in Cultured Primary Human Endothelial Cells by CRISPR/Cas9. Circulation Research 2015, 117: 121-128. PMID: 25940550, PMCID: PMC4490936, DOI: 10.1161/circresaha.117.306290.Peer-Reviewed Original ResearchAnimalsCD4-Positive T-LymphocytesCell SeparationCells, CulturedCRISPR-Cas SystemsEndothelial Progenitor CellsFemaleFetal BloodGene DeletionGene Knockout TechniquesGenes, MHC Class IIGenetic VectorsHLA-DR AntigensHumansIntracellular Signaling Peptides and ProteinsLentivirusLymphocyte ActivationLymphocyte Culture Test, MixedMiceMice, SCIDNuclear ProteinsPrimary Cell CultureProteinsTetracyclineTrans-ActivatorsVesicular Transport ProteinsTumor Necrosis Factor Disrupts Claudin-5 Endothelial Tight Junction Barriers in Two Distinct NF-κB-Dependent Phases
Clark PR, Kim RK, Pober JS, Kluger MS. Tumor Necrosis Factor Disrupts Claudin-5 Endothelial Tight Junction Barriers in Two Distinct NF-κB-Dependent Phases. PLOS ONE 2015, 10: e0120075. PMID: 25816133, PMCID: PMC4376850, DOI: 10.1371/journal.pone.0120075.Peer-Reviewed Original ResearchCell Membrane PermeabilityCells, CulturedClaudin-5DermisEndothelium, VascularHuman Umbilical Vein Endothelial CellsHumansMicroscopy, FluorescenceMyosin Light ChainsMyosin-Light-Chain KinaseNF-kappa BPhosphorylationRho-Associated KinasesRNA, Small InterferingSignal TransductionTight JunctionsTumor Necrosis Factor-alpha
2013
A composite model of the human postcapillary venule for investigation of microvascular leukocyte recruitment
Lauridsen HM, Pober JS, Gonzalez AL. A composite model of the human postcapillary venule for investigation of microvascular leukocyte recruitment. The FASEB Journal 2013, 28: 1166-1180. PMID: 24297702, PMCID: PMC3929680, DOI: 10.1096/fj.13-240986.Peer-Reviewed Original ResearchConceptsAdhesion molecule-1Cell adhesion molecule-1Molecule-1Endothelial cellsPostcapillary venulesBasement membraneVascular cell adhesion molecule-1Intercellular adhesion molecule-1Tumor necrosis factor αMicrovascular leukocyte recruitmentNecrosis factor αLate antigen-4Platelet endothelial cell adhesion molecule-1TNF-α activationInflammatory cascadeAntigen-4Neutrophil extravasationInterleukin-8Leukocyte recruitmentNeutrophil adhesionFactor αTNFPericytesVenular shear stressAnti-CD99Alloantibody and Complement Promote T Cell–Mediated Cardiac Allograft Vasculopathy Through Noncanonical Nuclear Factor-&kgr;B Signaling in Endothelial Cells
Jane-wit D, Manes TD, Yi T, Qin L, Clark P, Kirkiles-Smith NC, Abrahimi P, Devalliere J, Moeckel G, Kulkarni S, Tellides G, Pober JS. Alloantibody and Complement Promote T Cell–Mediated Cardiac Allograft Vasculopathy Through Noncanonical Nuclear Factor-&kgr;B Signaling in Endothelial Cells. Circulation 2013, 128: 2504-2516. PMID: 24045046, PMCID: PMC3885874, DOI: 10.1161/circulationaha.113.002972.Peer-Reviewed Original ResearchConceptsCardiac allograft vasculopathyPanel reactive antibodyNuclear factor-κB signalingFactor-κB signalingAllograft vasculopathyT cellsEndothelial cellsMembrane attack complexAlloreactive T cell activationChronic antibody-mediated rejectionNoncanonical nuclear factorProinflammatory gene programAntibody-mediated rejectionDonor-specific antibodiesGraft endothelial cellsLate allograft lossAlloreactive T cellsAllogeneic endothelial cellsT cell activationAttack complexHuman T cellsAllograft lossHeart transplantationTransplantation patientsLesion pathogenesis
2009
Generation of NO by Bystander Human CD8 T Cells Augments Allogeneic Responses by Inhibiting Cytokine Deprivation-Induced Cell Death
Choy JC, Pober JS. Generation of NO by Bystander Human CD8 T Cells Augments Allogeneic Responses by Inhibiting Cytokine Deprivation-Induced Cell Death. American Journal Of Transplantation 2009, 9: 2281-2291. PMID: 19663890, PMCID: PMC3505447, DOI: 10.1111/j.1600-6143.2009.02771.x.Peer-Reviewed Original ResearchConceptsHuman CD8 T cellsCD8 T cellsInducible NO synthaseT cellsActivated T cellsNitric oxideDeprivation-induced cell deathCell deathAllogeneic endothelial cellsT cell proliferationActivation-induced cell deathCytokine deprivationGeneration of NOT cell deathExogenous nitric oxideHuman T cellsNO augmentsAllogeneic responseS-nitrosylationNO synthaseProtective effectActivity of caspasesEndothelial cellsPharmacological inhibitorsDeath
2001
TNF Signaling in Vascular Endothelial Cells
Madge L, Pober J. TNF Signaling in Vascular Endothelial Cells. Experimental And Molecular Pathology 2001, 70: 317-325. PMID: 11418010, DOI: 10.1006/exmp.2001.2368.Peer-Reviewed Original ResearchConceptsTumor necrosis factorEndothelial cellsProinflammatory cytokine tumor necrosis factorCytokines tumor necrosis factorCultured human endothelial cellsVascular endothelial cellsHuman endothelial cellsNecrosis factorVascular endotheliumIntracellular pathwaysMajor targetTNF signalingCell typesCellsSuppression of Vascular Endothelial Growth Factor-Mediated Endothelial Cell Protection by Survivin Targeting
Mesri M, Morales-Ruiz M, Ackermann E, Bennett C, Pober J, Sessa W, Altieri D. Suppression of Vascular Endothelial Growth Factor-Mediated Endothelial Cell Protection by Survivin Targeting. American Journal Of Pathology 2001, 158: 1757-1765. PMID: 11337373, PMCID: PMC1891951, DOI: 10.1016/s0002-9440(10)64131-4.Peer-Reviewed Original ResearchApoptosisCell MovementCells, CulturedDNADNA, AntisenseDose-Response Relationship, DrugEndothelial Growth FactorsEndothelium, VascularGene Expression RegulationHumansInhibitor of Apoptosis ProteinsLymphokinesMicrotubule-Associated ProteinsNeoplasm ProteinsProteinsRNA, MessengerSurvivinVascular Endothelial Growth Factor AVascular Endothelial Growth FactorsHuman Vascular Endothelial Cells Stimulate a Lower Frequency of Alloreactive CD8+ Pre-CTL and Induce Less Clonal Expansion than Matching B Lymphoblastoid Cells: Development of a Novel Limiting Dilution Analysis Method Based on CFSE Labeling of Lymphocytes
Dengler T, Johnson D, Pober J. Human Vascular Endothelial Cells Stimulate a Lower Frequency of Alloreactive CD8+ Pre-CTL and Induce Less Clonal Expansion than Matching B Lymphoblastoid Cells: Development of a Novel Limiting Dilution Analysis Method Based on CFSE Labeling of Lymphocytes. The Journal Of Immunology 2001, 166: 3846-3854. PMID: 11238628, DOI: 10.4049/jimmunol.166.6.3846.Peer-Reviewed Original ResearchAntigens, CDB-Lymphocyte SubsetsCD8-Positive T-LymphocytesCell DivisionCell Line, TransformedCells, CulturedClone CellsCoculture TechniquesColony-Forming Units AssayCytotoxicity Tests, ImmunologicEndothelium, VascularFlow CytometryFluoresceinsFluorescent DyesHumansImmunologic MemoryInterphaseIsoantigensLymphocyte ActivationLymphocyte CountStem CellsSuccinimidesT-Lymphocyte SubsetsT-Lymphocytes, Regulatory
2000
Caveolin-1 Associates with TRAF2 to Form a Complex That Is Recruited to Tumor Necrosis Factor Receptors*
Feng X, Gaeta M, Madge L, Yang J, Bradley J, Pober J. Caveolin-1 Associates with TRAF2 to Form a Complex That Is Recruited to Tumor Necrosis Factor Receptors*. Journal Of Biological Chemistry 2000, 276: 8341-8349. PMID: 11112773, DOI: 10.1074/jbc.m007116200.Peer-Reviewed Original ResearchConceptsCaveolin-1Confocal fluorescence microscopyIntracellular regionNecrosis factor receptor-associated factor 2TNF receptor 2Receptor-associated factor 2TNF receptor 1Promoter-reporter geneCaveolin-1 associatesFluorescence microscopyProtein caveolin-1Caveolin-1 proteinHuman embryonic kidney 293 cellsIntracellular adapter proteinEmbryonic kidney 293 cellsAbsence of ligandRegions of enrichmentKidney 293 cellsEndogenous TRAF2HEK-293 cellsAdapter proteinCultured human umbilical vein endothelial cellsHuman umbilical vein endothelial cellsPlasma membraneUmbilical vein endothelial cellsSelective Inhibition of NF-κB Activation by a Peptide That Blocks the Interaction of NEMO with the IκB Kinase Complex
May M, D'Acquisto F, Madge L, Glöckner J, Pober J, Ghosh S. Selective Inhibition of NF-κB Activation by a Peptide That Blocks the Interaction of NEMO with the IκB Kinase Complex. Science 2000, 289: 1550-1554. PMID: 10968790, DOI: 10.1126/science.289.5484.1550.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsAnti-Inflammatory Agents, Non-SteroidalCells, CulturedCOS CellsEndothelium, VascularE-SelectinGene Expression RegulationHeLa CellsHumansI-kappa B KinaseInflammationMiceMice, Inbred C57BLMolecular Sequence DataMutationNF-kappa BPeptidesPoint MutationProtein Serine-Threonine KinasesProtein Structure, TertiaryRecombinant Fusion ProteinsConceptsNF-kappaBBasal NF-kappaB activityExperimental mouse modelTranscription factor nuclear factorCytokine-induced NF-kappaB activationCell-permeable NBD peptideInhibitor of kappaBNF-κB activationNF-kappaB activityNF-kappaB activationAssociation of NEMOIKK complexAcute inflammationDevelopment of drugsProinflammatory activationInflammatory responseNBD peptideMouse modelProinflammatory stimuliIκB kinase (IKK) complexNuclear factorRegulatory protein NEMOInflammationSelective inhibitionExpression of genesThe Death Domain of Tumor Necrosis Factor Receptor 1 Is Necessary but Not Sufficient for Golgi Retention of the Receptor and Mediates Receptor Desensitization
Gaeta M, Johnson D, Kluger M, Pober J. The Death Domain of Tumor Necrosis Factor Receptor 1 Is Necessary but Not Sufficient for Golgi Retention of the Receptor and Mediates Receptor Desensitization. Laboratory Investigation 2000, 80: 1185-1194. PMID: 10950109, DOI: 10.1038/labinvest.3780126.Peer-Reviewed Original ResearchConceptsDeath domainGolgi retentionPlasma membraneC-terminal death domainGolgi apparatusNF-kappaBDominant negative inhibitorWild-type receptorDisparate localizationTNF responseIntracellular domainC-terminusEndothelial cellsNegative inhibitorTNF signalsWild typeTumor necrosis factor receptor 1Chimeric receptorsFactor receptor 1Necrosis factor receptor 1Endogenous receptorsBasal expressionReceptor moleculesType receptorTNF actionIn vivo formation of complex microvessels lined by human endothelial cells in an immunodeficient mouse
Schechner J, Nath A, Zheng L, Kluger M, Hughes C, Sierra-Honigmann M, Lorber M, Tellides G, Kashgarian M, Bothwell A, Pober J. In vivo formation of complex microvessels lined by human endothelial cells in an immunodeficient mouse. Proceedings Of The National Academy Of Sciences Of The United States Of America 2000, 97: 9191-9196. PMID: 10890921, PMCID: PMC16844, DOI: 10.1073/pnas.150242297.Peer-Reviewed Original ResearchHuman Vascular Endothelial Cells Stimulate Memory But Not Naive CD8+ T Cells to Differentiate into CTL Retaining an Early Activation Phenotype
Dengler T, Pober J. Human Vascular Endothelial Cells Stimulate Memory But Not Naive CD8+ T Cells to Differentiate into CTL Retaining an Early Activation Phenotype. The Journal Of Immunology 2000, 164: 5146-5155. PMID: 10799873, DOI: 10.4049/jimmunol.164.10.5146.Peer-Reviewed Original ResearchMeSH KeywordsB-LymphocytesCD8-Positive T-LymphocytesCell DifferentiationCells, CulturedCoculture TechniquesCyclosporineCytotoxicity Tests, ImmunologicEndothelium, VascularHistocompatibility Antigens Class IHumansImmunologic MemoryImmunophenotypingInterleukin-12InterphaseLeukocyte Common AntigensLymphocyte ActivationT-Lymphocyte SubsetsT-Lymphocytes, CytotoxicConceptsB lymphoblastoid cellsT cellsNaive CD8Endothelial cellsImmunoregulatory cell typesIntracellular perforin contentAlloreactive T cellsAnti-CD28 mAbHuman vascular endothelial cellsHigh surface expressionVascular endothelial cellsExpansion of memoryConventional CTLGraft parenchymaGraft rejectionMemory CD8CTL generationPerforin contentCTL expansionVascular injuryHuman CD8CD40 ligandAlloreactive CTLAnatomic compartmentsICAM-1Cytoprotection of Human Umbilical Vein Endothelial Cells Against Apoptosis and CTL-Mediated Lysis Provided by Caspase-Resistant Bcl-2 Without Alterations in Growth or Activation Responses
Zheng L, Dengler T, Kluger M, Madge L, Schechner J, Maher S, Pober J, Bothwell A. Cytoprotection of Human Umbilical Vein Endothelial Cells Against Apoptosis and CTL-Mediated Lysis Provided by Caspase-Resistant Bcl-2 Without Alterations in Growth or Activation Responses. The Journal Of Immunology 2000, 164: 4665-4671. PMID: 10779771, DOI: 10.4049/jimmunol.164.9.4665.Peer-Reviewed Original ResearchMeSH KeywordsApoptosisCaspasesCell DivisionCell Line, TransformedCells, CulturedCulture Media, ConditionedCytotoxicity, ImmunologicEndothelial Growth FactorsEndothelium, VascularGenetic VectorsGreen Fluorescent ProteinsHumansLuminescent ProteinsProto-Oncogene Proteins c-bcl-2RetroviridaeT-Lymphocytes, CytotoxicTransduction, GeneticTransfectionUmbilical VeinsConceptsGraft endothelial cellsAllograft rejectionBcl-2Endothelial cellsAcute allograft rejectionClass I MHC moleculesNF-kappaB activationHuman umbilical vein endothelial cellsI MHC moleculesUmbilical vein endothelial cellsHost CTLVein endothelial cellsEndothelial injuryAnti-apoptotic gene Bcl-2MHC moleculesGene Bcl-2Induction of apoptosisBcl-2-transduced cellsClass IActivation responseApoptotic effectsCTLHUVECTNFGrowth factor withdrawalA Phosphatidylinositol 3-Kinase/Akt Pathway, Activated by Tumor Necrosis Factor or Interleukin-1, Inhibits Apoptosis but Does Not Activate NFκB in Human Endothelial Cells*
Madge L, Pober J. A Phosphatidylinositol 3-Kinase/Akt Pathway, Activated by Tumor Necrosis Factor or Interleukin-1, Inhibits Apoptosis but Does Not Activate NFκB in Human Endothelial Cells*. Journal Of Biological Chemistry 2000, 275: 15458-15465. PMID: 10748004, DOI: 10.1074/jbc.m001237200.Peer-Reviewed Original ResearchMeSH KeywordsAndrostadienesApoptosisCells, CulturedChromonesCulture Media, Serum-FreeEndothelium, VascularEnzyme ActivationEnzyme InhibitorsHumansInterleukin-1KineticsMorpholinesNF-kappa BPhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesProtein-Tyrosine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktRecombinant ProteinsTumor Necrosis Factor-alphaUmbilical VeinsWortmanninConceptsHuman endothelial cellsProtein kinaseStress-activated protein kinaseAkt pathwayMitogen-activated protein kinaseProtein kinase AktPromoter-reporter geneInhibitor of phosphatidylinositolEndothelial cellsSerum-deprived endothelial cellsPhosphorylation of AktGrowth factorAnti-apoptotic pathwaysKinase AktGene productsAnti-apoptotic effectsInhibits ApoptosisSerum deprivationAktLY294002Phospho-AktPro-inflammatory gene productsTranscriptionKinasePhosphatidylinositol