2024
SRF SUMOylation modulates smooth muscle phenotypic switch and vascular remodeling
Xu Y, Zhang H, Chen Y, Pober J, Zhou M, Zhou J, Min W. SRF SUMOylation modulates smooth muscle phenotypic switch and vascular remodeling. Nature Communications 2024, 15: 6919. PMID: 39134547, PMCID: PMC11319592, DOI: 10.1038/s41467-024-51350-5.Peer-Reviewed Original ResearchConceptsVascular smooth muscle cellsSerum response factorCardiovascular diseaseVSMC synthetic phenotypeVascular remodelingNeointimal formationSENP1 deficiencySerum response factor activitySmooth muscle phenotypic switchingPhenotypic switchingPathogenesis of cardiovascular diseaseSmooth muscle cellsPost-translational SUMOylationTreatment of cardiovascular diseasesInhibitor AZD6244Phospho-ELK1Increased nuclear accumulationLysosomal localizationGene transcriptionNuclear accumulationMuscle cellsCoronary arteryCVD patientsVSMC phenotypic switchTherapeutic potential
2022
Co-Expression and Functional Interactions of Death Receptor 3 and E-Selectin in Clear Cell Renal Cell Carcinoma
Al-Lamki RS, Wang J, Pober JS, Bradley JR. Co-Expression and Functional Interactions of Death Receptor 3 and E-Selectin in Clear Cell Renal Cell Carcinoma. American Journal Of Pathology 2022, 192: 722-736. PMID: 35063404, DOI: 10.1016/j.ajpath.2021.12.010.Peer-Reviewed Original ResearchConceptsMitogen-activated protein kinaseCell cycle entryCcRCC cellsDeath receptor 3Protein kinaseClear cell renal cell carcinoma cellsProximity ligation assayRenal cell carcinoma cellsReceptor 3E-selectinPotential new targetsCycle entryNF-κB-dependent mannerNF-κBLigation assayTumor gradeCcRCC tissuesFunctional interactionSelectin expressionFunctional roleClear cell renal cell carcinomaOrgan cultureCell renal cell carcinomaExpression increasesAddition of TL1A
2021
Coronavirus Disease 2019 (COVID-19) Coronary Vascular Thrombosis Correlation with Neutrophil but Not Endothelial Activation
Johnson JE, McGuone D, Xu ML, Jane-Wit D, Mitchell RN, Libby P, Pober JS. Coronavirus Disease 2019 (COVID-19) Coronary Vascular Thrombosis Correlation with Neutrophil but Not Endothelial Activation. American Journal Of Pathology 2021, 192: 112-120. PMID: 34599881, PMCID: PMC8479934, DOI: 10.1016/j.ajpath.2021.09.004.Peer-Reviewed Original ResearchConceptsVascular cell adhesion molecule-1Intracellular adhesion molecule-1Adhesion molecule-1Von Willebrand factorEndothelial activationMolecule-1Severe coronavirus disease 2019Neutrophil extracellular trap formationCell adhesion molecule-1COVID-19 cohortCOVID-19 patientsNeutrophil-platelet aggregatesCoronavirus disease 2019Extracellular trap formationCOVID-19Transcription factor p65Extensive thrombosisLymphocytic infiltrationMyocardial injuryThrombotic diathesisInflammatory activationNeutrophil activationCardiovascular diseaseDisease 2019Autopsy tissueDifferential inflammatory responses of the native left and right ventricle associated with donor heart preservation
Lei I, Huang W, Ward PA, Pober JS, Tellides G, Ailawadi G, Pagani FD, Landstrom AP, Wang Z, Mortensen RM, Cascalho M, Platt J, Chen Y, Lam HYK, Tang PC. Differential inflammatory responses of the native left and right ventricle associated with donor heart preservation. Physiological Reports 2021, 9: e15004. PMID: 34435466, PMCID: PMC8387788, DOI: 10.14814/phy2.15004.Peer-Reviewed Original ResearchConceptsRight ventricleCold ischemiaIL-10Inflammatory responseIL-6 protein levelsCold ischemic preservationEx vivo ischemiaLeft ventricle dysfunctionCold ischemic timeDonor heart preservationInflammatory cytokine expressionCell deathDifferential inflammatory responseTumor necrosis factorComparable inflammatory responsesHuman donor heartsCaspase-3 expressionIschemic preservationVentricle dysfunctionInflammasome expressionIschemic timeRNA sequencingContractile dysfunctionDonor heartsWarm perfusion
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
2016
Eculizumab Therapy for Chronic Antibody‐Mediated Injury in Kidney Transplant Recipients: A Pilot Randomized Controlled Trial
Kulkarni S, Kirkiles‐Smith N, Deng YH, Formica RN, Moeckel G, Broecker V, Bow L, Tomlin R, Pober JS. Eculizumab Therapy for Chronic Antibody‐Mediated Injury in Kidney Transplant Recipients: A Pilot Randomized Controlled Trial. American Journal Of Transplantation 2016, 17: 682-691. PMID: 27501352, DOI: 10.1111/ajt.14001.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAgedAntibodies, Monoclonal, HumanizedChronic DiseaseComplement C5Complement Inactivating AgentsEarly Intervention, EducationalFemaleFollow-Up StudiesGlomerular Filtration RateGraft RejectionGraft SurvivalHumansIsoantibodiesKidney Failure, ChronicKidney Function TestsKidney TransplantationLiving DonorsMaleMiddle AgedPilot ProjectsPrognosisRisk FactorsTissue DonorsTransplant RecipientsYoung AdultConceptsDe novo donor-specific antibodiesComplement inhibitionTreatment groupsNovo donor-specific antibodiesAntibody-Mediated InjuryC1q-positive patientsDonor-specific antibodiesKidney transplant recipientsPrimary end pointEndothelial cell injuryMo of observationEculizumab therapyEculizumab treatmentHumoral injuryTransplant recipientsKidney transplantRenal functionKidney functionChronic settingEGFR trajectoriesTreatment periodCell injuryPatientsEnd pointPercentage change
2013
Paracrine exchanges of molecular signals between alginate-encapsulated pericytes and freely suspended endothelial cells within a 3D protein gel
Andrejecsk JW, Cui J, Chang WG, Devalliere J, Pober JS, Saltzman WM. Paracrine exchanges of molecular signals between alginate-encapsulated pericytes and freely suspended endothelial cells within a 3D protein gel. Biomaterials 2013, 34: 8899-8908. PMID: 23973174, PMCID: PMC3839675, DOI: 10.1016/j.biomaterials.2013.08.008.Peer-Reviewed Original ResearchConceptsHuman umbilical vein endothelial cellsParacrine signalsFunctioning of tissuesProper survivalEndothelial cellsUmbilical vein endothelial cellsMolecular signalsRegulated deliveryVein endothelial cellsVessel-like structuresLiving cellsProtein gelsHepatocyte growth factorTherapeutic proteinsParacrine exchangesGrowth factorMicrovascular pericytesProteinAngiogenic proteinsCellsVascular tissue engineeringHUVEC behaviorTissue constructsPericytesLocal environment
1998
Endothelial cells in physiology and in the pathophysiology of vascular disorders.
Cines DB, Pollak ES, Buck CA, Loscalzo J, Zimmerman GA, McEver RP, Pober JS, Wick TM, Konkle BA, Schwartz BS, Barnathan ES, McCrae KR, Hug BA, Schmidt AM, Stern DM. Endothelial cells in physiology and in the pathophysiology of vascular disorders. Blood 1998, 91: 3527-61. PMID: 9572988.Peer-Reviewed Original ResearchAnimalsArteriosclerosisBlood CellsBlood CoagulationCell AdhesionCell Adhesion MoleculesCell DifferentiationCells, CulturedEndothelial Growth FactorsEndothelinsEndothelium, VascularEpoprostenolExtracellular MatrixFemaleFibrinolysisFibroblast Growth Factor 2HemodynamicsHumansInflammationLymphokinesMaleMiceNeovascularization, PhysiologicNitric OxidePlatelet Activating FactorPre-EclampsiaPregnancyThrombosisUmbilical VeinsVascular DiseasesVascular Endothelial Growth Factor AVascular Endothelial Growth Factors
1991
Expression of endothelial leukocyte adhesion molecule-1 in septic but not traumatic/hypovolemic shock in the baboon.
Redl H, Dinges HP, Buurman WA, van der Linden CJ, Pober JS, Cotran RS, Schlag G. Expression of endothelial leukocyte adhesion molecule-1 in septic but not traumatic/hypovolemic shock in the baboon. American Journal Of Pathology 1991, 139: 461-6. PMID: 1714243, PMCID: PMC1886066.Peer-Reviewed Original ResearchConceptsEndothelial leukocyte adhesion molecule-1Leukocyte adhesion molecule-1Hypovolemic shockSeptic shockAdhesion molecule-1Endothelial leukocyte adhesion molecule-1 expressionMolecule-1Adhesion molecule-1 expressionGranulocyte elastase levelsMolecule-1 expressionELAM-1 expressionTumor necrosis factorDe novo expressionEndothelial activationElastase levelsLive Escherichia coliNeutrophil activationNecrosis factorImmunohistochemical techniquesELAM-1ELAM expressionStrong stainingNovo expressionSmall veinsHigh levels
1989
ENDOTHELIAL CELL ACTIVATION AND HIGH INTERLEUKIN-1 SECRETION IN THE PATHOGENESIS OF ACUTE KAWASAKI DISEASE
Leung D, Kurt-Jones E, Newburger J, Cotran R, Burns J, Pober J. ENDOTHELIAL CELL ACTIVATION AND HIGH INTERLEUKIN-1 SECRETION IN THE PATHOGENESIS OF ACUTE KAWASAKI DISEASE. The Lancet 1989, 334: 1298-1302. PMID: 2480498, DOI: 10.1016/s0140-6736(89)91910-7.Peer-Reviewed Original ResearchMeSH KeywordsAntigens, SurfaceCell AdhesionCell Adhesion MoleculesChild, PreschoolEndothelium, VascularE-SelectinFemaleGamma-GlobulinsHLA-DQ AntigensHumansImmunization, PassiveIntercellular Adhesion Molecule-1Interleukin-1MaleMembrane GlycoproteinsMucocutaneous Lymph Node SyndromeReceptors, ImmunologicSkinConceptsEndothelial cell activationCoronary artery abnormalitiesCell activationInterleukin-1Gammaglobulin treatmentArtery abnormalitiesKawasaki diseaseAcute Kawasaki disease patientsPeripheral blood mononuclear cellsEndothelial cellsCytotoxic antibody activityIntravenous gammaglobulin treatmentKawasaki disease patientsAcute Kawasaki diseaseEndothelial cell antigensBlood mononuclear cellsInterleukin-1 secretionTumor necrosis factorIL-1 secretionEndothelial cell expressionSkin biopsy samplesMeans of immunoperoxidaseMucocutaneous symptomsPersistent feverClinical symptomsTumor necrosis factor and interferon-gamma induce distinct patterns of endothelial activation and associated leukocyte accumulation in skin of Papio anubis.
Munro JM, Pober JS, Cotran RS. Tumor necrosis factor and interferon-gamma induce distinct patterns of endothelial activation and associated leukocyte accumulation in skin of Papio anubis. American Journal Of Pathology 1989, 135: 121-33. PMID: 2505619, PMCID: PMC1880213.Peer-Reviewed Original ResearchConceptsLeukocyte accumulationNecrosis factorIFN-gammaEndothelial cell antigen expressionAdhesion moleculesAnti-intercellular adhesion moleculeEndothelial cell hypertrophyPolymorphonuclear leukocyte accumulationTumor necrosis factorCytokine-activated endotheliumLeukocyte adhesion moleculesCell antigen expressionImmune inflammationEndothelial activationLeukocyte infiltrationHypersensitivity reactionsMononuclear cellsHLA-DPEnvelope antigenAntigen expressionVascular permeabilitySubsequent extravasationRecombinant human interferonCell hypertrophyEndothelial morphology
1988
LYTIC ANTI-ENDOTHELIAL CELL ANTIBODIES IN HAEMOLYTIC-URAEMIC SYNDROME
Leung D, Havens P, Moake J, Kim M, Pober J. LYTIC ANTI-ENDOTHELIAL CELL ANTIBODIES IN HAEMOLYTIC-URAEMIC SYNDROME. The Lancet 1988, 332: 183-186. PMID: 2899661, DOI: 10.1016/s0140-6736(88)92287-8.Peer-Reviewed Original ResearchConceptsAnti-endothelial cell antibodiesHaemolytic uraemic syndromeThrombotic thrombocytopenic purpuraCell antibodiesComplement-fixing IgGDisorder of immunoregulationAnti-endothelial antibodiesEndothelial cell antigensCultured human umbilical vein endothelial cellsGamma-interferon treatmentHuman umbilical vein endothelial cellsUmbilical vein endothelial cellsAdult patientsVein endothelial cellsThrombocytopenic purpuraIgM antibodiesVascular injuryInterferon treatmentUraemic syndromeGamma interferonCell antigensControl seraEndothelial cellsAntibodiesSerum
1987
Induction of an activation antigen on postcapillary venular endothelium in human skin organ culture.
Messadi DV, Pober JS, Fiers W, Gimbrone MA, Murphy GF. Induction of an activation antigen on postcapillary venular endothelium in human skin organ culture. The Journal Of Immunology 1987, 139: 1557-62. PMID: 3497975, DOI: 10.4049/jimmunol.139.5.1557.Peer-Reviewed Original ResearchConceptsTumor necrosis factorActivation antigensNecrosis factorInterleukin-1Microvascular endotheliumEndothelial cellsEndothelial activation antigenMediators interleukin-1Postcapillary venular endotheliumCultured human umbilical vein endothelial cellsSuperficial vascular plexusOrgan cultureHuman skin organ cultureShort-term organ cultureHuman umbilical vein endothelial cellsSkin organ cultureUmbilical vein endothelial cellsVenular endothelial cellsMicrovascular stainingPostcapillary venular endothelial cellsVein endothelial cellsEndogenous cytokinesLymphocyte traffickingInterleukin-2Venular endothelium
1986
Two monokines, interleukin 1 and tumor necrosis factor, render cultured vascular endothelial cells susceptible to lysis by antibodies circulating during Kawasaki syndrome.
Leung DY, Geha RS, Newburger JW, Burns JC, Fiers W, Lapierre LA, Pober JS. Two monokines, interleukin 1 and tumor necrosis factor, render cultured vascular endothelial cells susceptible to lysis by antibodies circulating during Kawasaki syndrome. Journal Of Experimental Medicine 1986, 164: 1958-1972. PMID: 3491174, PMCID: PMC2188474, DOI: 10.1084/jem.164.6.1958.Peer-Reviewed Original ResearchConceptsAcute Kawasaki syndromeTumor necrosis factorKawasaki syndromeHuman endothelial cellsIL-1Cytotoxic antibodiesImmune activationEndothelial cellsNecrosis factorTarget antigenComplement-dependent cytotoxic activityAcute febrile illnessEndothelial cell antigensVascular smooth muscle cellsAge-matched controlsMonocytes/macrophagesSmooth muscle cellsCultured vascular endothelial cellsVascular endothelial cellsComplement-mediated killingDiffuse vasculitisConvalescent phaseFebrile illnessAcute phaseVascular injury
1979
Antibody-Mediated Aplastic Anemia and Diffuse Fasciitis
Hoffman R, Dainiak N, Sibrack L, Pober J, Waldron J. Antibody-Mediated Aplastic Anemia and Diffuse Fasciitis. New England Journal Of Medicine 1979, 300: 718-721. PMID: 763302, DOI: 10.1056/nejm197903293001307.Peer-Reviewed Original Research