2023
Endotheliopathy of liver sinusoidal endothelial cells in liver disease
Kondo R, Iwakiri Y, Kage M, Yano H. Endotheliopathy of liver sinusoidal endothelial cells in liver disease. Pathology International 2023, 73: 381-393. PMID: 37589433, DOI: 10.1111/pin.13361.Peer-Reviewed Original ResearchConceptsLiver diseaseSinusoidal endothelial cellsEndothelial cellsLiver injuryLiver tissueIntercellular adhesion molecule-1Improvement of thrombocytopeniaNeutrophil chemotactic mediatorsChronic hepatitis CLiver sinusoidal endothelial cellsSetting of inflammationSevere hepatic inflammationAdhesion molecule-1Largest solid organPotential therapeutic strategyVascular endothelial cellsVon Willebrand factorHepatitis CNeutrophil accumulationHepatic inflammationChemotactic mediatorsIL-6Antithrombotic factorsChemokine ligandSolid organsGenetic Variation in Intercellular Adhesion Molecule-1 (ICAM-1) and Diastolic Heart Failure in the Black Population in the United States
Mezue K, Driggin E. Genetic Variation in Intercellular Adhesion Molecule-1 (ICAM-1) and Diastolic Heart Failure in the Black Population in the United States. Journal Of Cardiac Failure 2023, 29: 1173-1174. PMID: 37062471, DOI: 10.1016/j.cardfail.2023.03.021.Peer-Reviewed Original ResearchConceptsIntercellular adhesion molecule-1Diastolic heart failureAdhesion molecule-1Genetic variationHeart failureMolecule-1The Effects of Pregnancy on the Pulmonary Immune Response in a Mouse Model of LPS-Induced Acute Lung Injury
Rieck R, Bivona J, Hoyt L, Ventrone S, Kokoszynska M, Bonney E, Suratt B. The Effects of Pregnancy on the Pulmonary Immune Response in a Mouse Model of LPS-Induced Acute Lung Injury. American Journal Of Perinatology 2023, 40: 817-824. PMID: 36796402, DOI: 10.1055/s-0043-1761916.Peer-Reviewed Original ResearchConceptsAcute lung injuryEffect of pregnancyNonpregnant miceAdhesion molecule-1Lung injuryPregnant miceNeutrophil responseImmune responseVCAM-1Mouse modelBronchoalveolar lavage fluid (BALF) differential cell countMolecule-1LPS-Induced Acute Lung InjuryPulmonary innate immune responseVascular cell adhesion molecule-1Intercellular adhesion molecule-1Cell adhesion molecule-1BALF total cellsBlood neutrophil responsesInhalation of lipopolysaccharidePulmonary immune responseVascular endothelial adhesion moleculesSevere lung diseasePeripheral blood neutrophilsBone marrow neutrophils
2020
Herpesvirus-infected Hofbauer cells activate endothelial cells through an IL-1β-dependent mechanism
Hendrix P, Tang Z, Silasi M, Racicot KE, Mor G, Abrahams VM, Guller S. Herpesvirus-infected Hofbauer cells activate endothelial cells through an IL-1β-dependent mechanism. Placenta 2020, 91: 59-65. PMID: 32174308, PMCID: PMC7078070, DOI: 10.1016/j.placenta.2020.01.010.Peer-Reviewed Original ResearchConceptsHuman umbilical vein endothelial cellsHofbauer cellsIL-1βAdhesion molecule-1Placental viral infectionsIL-8Viral infectionFetal inflammationEndothelial cellsE-selectinMolecule-1IL-1 receptor antagonistVascular adhesion molecule-1Intercellular adhesion molecule-1Adverse pregnancy outcomesMHV-68 infectionIL-1β secretionICAM-1 mRNAUmbilical vein endothelial cellsUmbilical endothelial cellsPregnancy outcomesVein endothelial cellsIL-1raPlacental macrophagesHUVEC expression
2019
ARHGAP18: A Flow‐Responsive Gene That Regulates Endothelial Cell Alignment and Protects Against Atherosclerosis
Lay AJ, Coleman PR, Formaz‐Preston A, Ting KK, Roediger B, Weninger W, Schwartz MA, Vadas MA, Gamble JR. ARHGAP18: A Flow‐Responsive Gene That Regulates Endothelial Cell Alignment and Protects Against Atherosclerosis. Journal Of The American Heart Association 2019, 8: e010057. PMID: 30630384, PMCID: PMC6497359, DOI: 10.1161/jaha.118.010057.Peer-Reviewed Original ResearchConceptsApolipoprotein EHigh-fat diet-induced modelIntercellular adhesion molecule-1Endothelial nitric oxide synthaseHigh-fat dietDevelopment of atherosclerosisNitric oxide synthaseDiet-induced modelAdhesion molecule-1Double mutant miceAortic diseaseAtherosclerosis developmentInflammatory phenotypeOxide synthaseMolecule-1AtherosclerosisEarly onsetProtective genesMiceFlow-responsive genesAtheroprotective regionsEndothelial cell alignmentAdaptive responseAnalysis of ECEC ability
2018
A novel method for segmenting growth of cells in sheared endothelial culture reveals the secretion of an anti-inflammatory mediator
Ghim M, Pang K, Arshad M, Wang X, Weinberg P. A novel method for segmenting growth of cells in sheared endothelial culture reveals the secretion of an anti-inflammatory mediator. Journal Of Biological Engineering 2018, 12: 15. PMID: 30127849, PMCID: PMC6092814, DOI: 10.1186/s13036-018-0107-6.Peer-Reviewed Original ResearchVascular cell adhesion molecule-1Intercellular adhesion molecule-1Adhesion molecule-1Molecule-1Cell adhesion molecule-1Anti-inflammatory mediatorsAnti-inflammatory effectsPathogenesis of atherosclerosisEndothelial cellsBlood vesselsNormal physiologyEndothelial culturesGrowth of cellsMediatorsConclusionsThe resultsEndothelium
2015
Na+/H+ exchanger regulatory factor 1 knockout mice have an attenuated hepatic inflammatory response and are protected from cholestatic liver injury
Li M, Mennone A, Soroka CJ, Hagey LR, Ouyang X, Weinman EJ, Boyer JL. Na+/H+ exchanger regulatory factor 1 knockout mice have an attenuated hepatic inflammatory response and are protected from cholestatic liver injury. Hepatology 2015, 62: 1227-1236. PMID: 26108984, PMCID: PMC4589453, DOI: 10.1002/hep.27956.Peer-Reviewed Original ResearchConceptsBile duct ligationLiver injuryInflammatory responseICAM-1BDL miceBDL-induced liver injuryNeutrophil-mediated liver injuryTotal bile acid concentrationTumor necrosis factor alphaIntercellular adhesion molecule-1Hepatic neutrophil accumulationAttenuated liver injuryCholestatic liver injuryHepatic inflammatory responseMouse liverSerum alanine aminotransferaseBile acid concentrationsHepatic inflammatory diseasesICAM-1 expressionNecrosis factor alphaAdhesion molecule-1Wild-type miceICAM-1 proteinNew therapeutic targetsMessenger RNA levels
2014
Pan-Selectin Antagonist Rivipansel (GMI-1070) Reduces Soluble E-Selectin Levels While Improving Clinical Outcomes in SCD Vaso-Occlusive Crisis
Wun T, Telen M, Krishnamurti L, McCavit T, DeCastro L, Flanner H, Kuypers F, Larkin S, Rhee S, Magnani J, Thackray H. Pan-Selectin Antagonist Rivipansel (GMI-1070) Reduces Soluble E-Selectin Levels While Improving Clinical Outcomes in SCD Vaso-Occlusive Crisis. Blood 2014, 124: 2704. DOI: 10.1182/blood.v124.21.2704.2704.Peer-Reviewed Original ResearchSoluble E-selectin levelsPhase 2 trialVaso-occlusive crisisSE-selE-selectin levelsClinical outcomesAdhesion molecule-1Placebo groupLast doseSubgroup analysisE-selectinMolecule-1Sickle cell disease vaso-occlusive crisisDouble-blind phase 2 trialSoluble adhesion molecules E-selectinBaseline white blood cell countRandomized phase 2 studySCD vaso-occlusive crisisSoluble adhesion molecule concentrationsAge groupsVascular cell adhesion molecule-1White blood cell countIntercellular adhesion molecule-1Adhesion molecules E-selectinCell adhesion molecule-1
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-CD99SOCS1 Prevents Graft Arteriosclerosis by Preserving Endothelial Cell Function
Qin L, Huang Q, Zhang H, Liu R, Tellides G, Min W, Yu L. SOCS1 Prevents Graft Arteriosclerosis by Preserving Endothelial Cell Function. Journal Of The American College Of Cardiology 2013, 63: 21-29. PMID: 23994402, PMCID: PMC3932325, DOI: 10.1016/j.jacc.2013.08.694.Peer-Reviewed Original ResearchConceptsAdhesion molecule-1Cell adhesion molecule-1Graft arteriosclerosisMolecule-1Aortic endothelial cellsEndothelial cellsEndothelial functionGA progressionNeointima formationLate cardiac allograft failureVascular cell adhesion molecule-1Intercellular adhesion molecule-1Cytokine-induced adhesion molecule expressionCardiac allograft failureNormal endothelial functionEndothelial inflammatory responseInflammatory cell infiltrationMouse aortic endothelial cellsAdhesion molecule expressionPlatelet/endothelial cell adhesion molecule-1Better vascular functionEndothelial cell adhesion molecule-1Cytokine-induced expressionEndothelial adhesion moleculesCultured aortic endothelial cells
2012
Soluble Vascular Cell Adhesion Molecule Levels, Endothelin-1 and Endothelial Nitric Oxide Synthase Gene Polymorphisms: Association with Clinical Symptoms in Sickle Cell Anemia.
Vilas-Boas W, Figueiredo C, Cerqueira B, Pitanga T, Zanette A, Reis M, Goncalves M. Soluble Vascular Cell Adhesion Molecule Levels, Endothelin-1 and Endothelial Nitric Oxide Synthase Gene Polymorphisms: Association with Clinical Symptoms in Sickle Cell Anemia. Blood 2012, 120: 2118. DOI: 10.1182/blood.v120.21.2118.2118.Peer-Reviewed Original ResearchAcute chest syndromeT gene polymorphismEndothelial nitric oxide synthaseSoluble adhesion moleculesAdhesion molecule-1Endothelin-1HbSS patientsENOS -786TGene polymorphismsMedical historyMolecule-1Vascular cell adhesion molecule levelsEndothelial nitric oxide synthase gene polymorphismsSoluble intercellular adhesion molecule-1Nitric oxide synthase gene polymorphismsC gene promoter polymorphismsCell adhesion molecule levelsNitric oxide synthesis pathwayVascular cell adhesion molecule-1Intercellular adhesion molecule-1Adhesion moleculesCell adhesion molecule-1Levels of sICAMAdhesion molecule levelsIncreased inflammatory stateMacrophage β2 Integrin–Mediated, HuR-Dependent Stabilization of Angiogenic Factor–Encoding mRNAs in Inflammatory Angiogenesis
Zhang J, Modi Y, Yarovinsky T, Yu J, Collinge M, Kyriakides T, Zhu Y, Sessa WC, Pardi R, Bender JR. Macrophage β2 Integrin–Mediated, HuR-Dependent Stabilization of Angiogenic Factor–Encoding mRNAs in Inflammatory Angiogenesis. American Journal Of Pathology 2012, 180: 1751-1760. PMID: 22322302, PMCID: PMC3349897, DOI: 10.1016/j.ajpath.2011.12.025.Peer-Reviewed Original ResearchMeSH KeywordsAngiogenesis Inducing AgentsAnimalsCD18 AntigensCell AdhesionCells, CulturedDisease Models, AnimalELAV ProteinsGene Expression RegulationGene Knockout TechniquesHindlimbInflammationIschemiaMacrophagesMiceMice, KnockoutMuscle, SkeletalNeovascularization, PathologicReal-Time Polymerase Chain ReactionRNA, MessengerConceptsKnockout miceAngiogenic factorsT cell cytokine productionIntercellular adhesion molecule-1Blood flow recoveryFemoral artery ligationLittermate wild-type controlsVascular endothelial growth factorBone marrow-derived macrophagesMatrix metalloproteinase-9Adhesion molecule-1Endothelial growth factorMarrow-derived macrophagesSoluble factor productionWild-type controlsArtery ligationLigand intercellular adhesion molecule-1Cytokine productionInflammatory angiogenesisMetalloproteinase-9Tissue ischemiaInflammatory stimuliMolecule-1Macrophage productionNeovascular response
2010
VEGF Blockade Inhibits Lymphocyte Recruitment and Ameliorates Immune-Mediated Vascular Remodeling
Zhang J, Silva T, Yarovinsky T, Manes TD, Tavakoli S, Nie L, Tellides G, Pober JS, Bender JR, Sadeghi MM. VEGF Blockade Inhibits Lymphocyte Recruitment and Ameliorates Immune-Mediated Vascular Remodeling. Circulation Research 2010, 107: 408-417. PMID: 20538685, PMCID: PMC2929975, DOI: 10.1161/circresaha.109.210963.Peer-Reviewed Original ResearchMeSH KeywordsAngiogenesis InhibitorsAnimalsAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedArteriesBevacizumabCD3 ComplexCoronary VesselsHumansJurkat CellsLymphocytesMiceMice, SCIDReceptors, Vascular Endothelial Growth FactorT-LymphocytesTransplantation, HeterologousVascular Endothelial Growth Factor AConceptsVascular endothelial growth factorRole of VEGFAdhesion molecule-1T cellsVascular remodelingHuman T cellsMolecule-1Recombinant intercellular adhesion molecule-1Human arteriesVascular cell adhesion molecule-1Intercellular adhesion molecule-1Cell adhesion molecule-1Inhibition of VEGFT cell accumulationPeripheral blood mononuclearEffects of VEGFSubpopulation of CD3Novel therapeutic approachesEndothelial growth factorT cell activationT cell linesVEGFR-1 mRNAT cell captureLymphocyte recruitmentBlood mononuclear
2009
Cutting Edge: TNF-Induced MicroRNAs Regulate TNF-Induced Expression of E-Selectin and Intercellular Adhesion Molecule-1 on Human Endothelial Cells: Feedback Control of Inflammation
Suárez Y, Wang C, Manes TD, Pober JS. Cutting Edge: TNF-Induced MicroRNAs Regulate TNF-Induced Expression of E-Selectin and Intercellular Adhesion Molecule-1 on Human Endothelial Cells: Feedback Control of Inflammation. The Journal Of Immunology 2009, 184: 21-25. PMID: 19949084, PMCID: PMC2797568, DOI: 10.4049/jimmunol.0902369.Peer-Reviewed Original ResearchMeSH KeywordsCells, CulturedE-SelectinEndothelial CellsFeedback, PhysiologicalGene ExpressionGene Expression RegulationHumansImmunohistochemistryInflammationIntercellular Adhesion Molecule-1MicroRNAsOligonucleotide Array Sequence AnalysisReverse Transcriptase Polymerase Chain ReactionTransfectionTumor Necrosis Factor-alphaConceptsEndothelial cellsGene expressionUntranslated regionHuman endothelial cellsMiRNAsCultured endothelial cellsTarget sequenceMicroRNA pairsNegative feedback controlMiR-31Adhesion moleculesCellsExpressionNeutrophil adhesionE-selectinAdhesion molecule-1AdhesionTransfectionIntercellular adhesion molecule-1MRNAMolecule-1SequenceEndothelial adhesion moleculesSpecific antagonismICAM-1
2007
Knockdown of TNFR1 by the sense strand of an ICAM-1 siRNA: dissection of an off-target effect
Clark PR, Pober JS, Kluger MS. Knockdown of TNFR1 by the sense strand of an ICAM-1 siRNA: dissection of an off-target effect. Nucleic Acids Research 2007, 36: 1081-1097. PMID: 18096615, PMCID: PMC2275081, DOI: 10.1093/nar/gkm630.Peer-Reviewed Original ResearchConceptsTumor necrosis factor receptor 1Endothelial cellsIntercellular adhesion molecule-1ICAM-1 siRNAAnti-TNF activityCultured human umbilical vein endothelial cellsICAM-1 expressionAdhesion molecule-1Off-target effectsNecrosis factor receptor 1Human umbilical vein ECHuman umbilical vein endothelial cellsFactor receptor 1Umbilical vein endothelial cellsExpression of mRNAIL-1 activationVein endothelial cellsLocal inflammationTNFR1 mRNANecrosis factorEarly TNFICAM-1VCAM-1E-selectinTransfection of ECs
2004
Stromal Cell–Derived Factor-1α Plays a Critical Role in Stem Cell Recruitment to the Heart After Myocardial Infarction but Is Not Sufficient to Induce Homing in the Absence of Injury
Abbott JD, Huang Y, Liu D, Hickey R, Krause DS, Giordano FJ. Stromal Cell–Derived Factor-1α Plays a Critical Role in Stem Cell Recruitment to the Heart After Myocardial Infarction but Is Not Sufficient to Induce Homing in the Absence of Injury. Circulation 2004, 110: 3300-3305. PMID: 15533866, DOI: 10.1161/01.cir.0000147780.30124.cf.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBenzylaminesBone Marrow CellsBone Marrow TransplantationCell LineageCell MovementChemokine CXCL12Chemokines, CXCCyclamsFemaleGene Expression ProfilingGene Expression RegulationGenetic TherapyHeterocyclic CompoundsIntercellular Adhesion Molecule-1Matrix Metalloproteinase 9MiceMice, Inbred NODMice, SCIDMyocardial InfarctionMyocardiumReceptors, CXCR4Recombinant Fusion ProteinsStem Cell TransplantationStem CellsTransduction, GeneticVascular Cell Adhesion Molecule-1Vascular Endothelial Growth Factor AConceptsBone marrow-derived cellsStromal cell-derived factor-1alphaMyocardial infarctionBMDC recruitmentAdhesion molecule-1Molecule-1Recruitment of BMDCsInfarcted heartSerum SDF-1 levelsVascular cell adhesion molecule-1Intercellular adhesion molecule-1Stromal cell-derived factor-1αCell adhesion molecule-1Administration of AMD3100SDF-1/CXCR4 interactionMarrow-derived cellsSDF-1 levelsAbsence of MIVascular endothelial growth factorMatrix metalloproteinase-9Sham-operated controlsSDF-1 mRNAEndothelial growth factorAbsence of injuryQuantitative polymerase chain reaction
2001
PR-39 and PR-11 peptides inhibit ischemia-reperfusion injury by blocking proteasome-mediated IκBα degradation
Bao J, Sato K, Li M, Gao Y, Abid R, Aird W, Simons M, Post M. PR-39 and PR-11 peptides inhibit ischemia-reperfusion injury by blocking proteasome-mediated IκBα degradation. AJP Heart And Circulatory Physiology 2001, 281: h2612-h2618. PMID: 11709430, DOI: 10.1152/ajpheart.2001.281.6.h2612.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnti-Bacterial AgentsAntimicrobial Cationic PeptidesCells, CulturedCysteine EndopeptidasesDNA-Binding ProteinsEndothelium, VascularHumansI-kappa B ProteinsIntercellular Adhesion Molecule-1MaleMultienzyme ComplexesMyocardial Reperfusion InjuryMyocardiumNADPH OxidasesNeutrophilsNF-KappaB Inhibitor alphaPeptide FragmentsPeroxidasePhosphoproteinsProteasome Endopeptidase ComplexRatsRats, Sprague-DawleyReactive Oxygen SpeciesUmbilical VeinsVascular Cell Adhesion Molecule-1Ventricular Function, LeftConceptsIschemia-reperfusion injuryB alpha degradationAdhesion molecule-1PR-11Alpha degradationNeutrophil infiltrationMyeloperoxidase activityInfarct sizeMolecule-1Vascular cell adhesion molecule-1Myocardial ischemia-reperfusion injuryIntercellular adhesion molecule-1Cell adhesion molecule-1Ventricular systolic pressureTime of reperfusionIschemia-reperfusion modelMin of ischemiaPR-39Controls 24 hBlood pressureSystolic pressureCardiac functionIntramyocardial injectionIκBα degradationAdhesion moleculesAn anti-CD11/CD18 monoclonal antibody in patients with acute myocardial infarction having percutaneous transluminal coronary angioplasty (the FESTIVAL study)
Rusnak J, Kopecky S, Clements I, Gibbons R, Holland A, Peterman H, Martin J, Saoud J, Feldman R, Breisblatt W, Simons M, Gessler C, Yu A, Investigators F. An anti-CD11/CD18 monoclonal antibody in patients with acute myocardial infarction having percutaneous transluminal coronary angioplasty (the FESTIVAL study). The American Journal Of Cardiology 2001, 88: 482-487. PMID: 11524054, DOI: 10.1016/s0002-9149(01)01723-4.Peer-Reviewed Original ResearchMeSH KeywordsAgedAngioplasty, Balloon, CoronaryAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedChi-Square DistributionCombined Modality TherapyCoronary AngiographyDose-Response Relationship, DrugDouble-Blind MethodDrug Administration ScheduleElectrocardiographyFemaleFollow-Up StudiesHumansInfusions, IntravenousMaleMiddle AgedMyocardial InfarctionNeuroprotective AgentsPilot ProjectsProbabilitySensitivity and SpecificitySeverity of Illness IndexStatistics, NonparametricSurvival RateTomography, Emission-Computed, Single-PhotonTreatment OutcomeConceptsPercutaneous transluminal coronary angioplastyAcute myocardial infarctionIntercellular adhesion molecule-1Hu23F2GTransluminal coronary angioplastyCD11/CD18Monoclonal antibodiesCoronary angioplastyMyocardial infarctionCD11/CD18 monoclonal antibodyMyocardial single photon emissionInitial clinical safetySubsequent cardiac interventionsST-segment elevationHumanized monoclonal antibodyActivation of neutrophilsAdhesion molecule-1CD18 monoclonal antibodySignificant differencesG treatment groupsNear-baseline valuesSingle photon emissionAdverse eventsCoronary reperfusionInflammatory mediatorsMacrophage migration inhibitory factor is an important mediator in the pathogenesis of gastric inflammation in rats
Huang X, Hui C, Chen Y, Chun B, Wong Y, Fung P, Metz C, Cho C, Hui W, Bucala R, Lam S, Lan H. Macrophage migration inhibitory factor is an important mediator in the pathogenesis of gastric inflammation in rats. Gastroenterology 2001, 121: 619-630. PMID: 11522746, DOI: 10.1053/gast.2001.27205.Peer-Reviewed Original ResearchMeSH KeywordsAcetic AcidAcute DiseaseAnimalsAntibodies, MonoclonalDisease Models, AnimalGastritisGene ExpressionIn Situ HybridizationIn Vitro TechniquesIntercellular Adhesion Molecule-1Macrophage Migration-Inhibitory FactorsMacrophagesMaleNeutrophilsNitric Oxide SynthaseNitric Oxide Synthase Type IIRatsRats, Sprague-DawleyRNA, MessengerStomach UlcerTumor Necrosis Factor-alphaWound HealingConceptsAcute gastric ulcerMigration inhibitory factorInducible nitric oxide synthaseGastric ulcerNitric oxide synthaseGastric inflammationMIF antibodyOxide synthaseRole of MIFRat gastric ulcer modelsInhibitory factorMacrophage migration inhibitory factorIntercellular adhesion molecule-1Tumor necrosis factor alphaGastric ulcer modelImmune-mediated diseasesKey inflammatory mediatorsMajor inflammatory cellsAccumulation of macrophagesNecrosis factor alphaAdhesion molecule-1Sites of inflammationNeutrophil accumulationMIF productionUlcer size
1999
Herpes Simplex Virus (HSV)-Mediated ICAM-1 Gene Transfer Abrogates Tumorigenicity and Induces Anti-Tumor Immunity
D’Angelica M, Tung C, Allen P, Halterman M, Delman K, Delohery T, Klimstra D, Brownlee M, Federoff H, Fong Y. Herpes Simplex Virus (HSV)-Mediated ICAM-1 Gene Transfer Abrogates Tumorigenicity and Induces Anti-Tumor Immunity. Molecular Medicine 1999, 5: 606-616. PMID: 10551902, PMCID: PMC2230459, DOI: 10.1007/bf03402073.Peer-Reviewed Original ResearchConceptsIntercellular adhesion molecule-1Surface expression of adhesion moleculesExpression of adhesion moleculesTumor cellsCell surface expressionAmplicon vectorsAdhesion moleculesHigh-level cell surface expressionInduce anti-tumor immunityTransplantable rat hepatocellular carcinomaCell surface ICAM-1 expressionSurface expressionCell surface expression of adhesion moleculesExposure of tumor cellsExpression of intercellular adhesion molecule-1Immune response to cancerSurface ICAM-1 expressionAnti-tumor immunityAnti-tumor responsesParental tumor cellsHuman colorectal cancer cell linesHuman intercellular adhesion molecule-1Increased tumor expressionICAM-1 expressionHerpes simplex virus
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