2012
Macrophage 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
2002
Integrin‐dependent regulation of gene expression in leukocytes
Rossetti G, Collinge M, Molteni R, Bender J, Pardi R. Integrin‐dependent regulation of gene expression in leukocytes. Immunological Reviews 2002, 186: 189-207. PMID: 12234372, DOI: 10.1034/j.1600-065x.2002.18616.x.Peer-Reviewed Original ResearchConceptsIntegrin engagementGene expression regulationIntegrin-dependent regulationCell cycle restriction pointExpression regulationNumerous genesTransduce signalsMatrix degrading proteinsTranscriptional activationGenetic programTranscription modulatorsIntegrin-dependent mechanismJAK-STATsGene expressionIntercellular adhesionDegrading proteinsCell differentiationAlphaLbeta2 integrinJab-1Restriction pointMRNA transcriptsT cell differentiationEnvironmental stimuliPotent signalCell phenotype
2001
INHIBITION OF INTERFERON-γ–MEDIATED MICROVASCULAR ENDOTHELIAL CELL MAJOR HISTOCOMPATIBILITY COMPLEX CLASS II GENE ACTIVATION BY HMG-COA REDUCTASE INHIBITORS1
Sadeghi M, Tiglio A, Sadigh K, O’Donnell L, Collinge M, Pardi R, Bender J. INHIBITION OF INTERFERON-γ–MEDIATED MICROVASCULAR ENDOTHELIAL CELL MAJOR HISTOCOMPATIBILITY COMPLEX CLASS II GENE ACTIVATION BY HMG-COA REDUCTASE INHIBITORS1. Transplantation 2001, 71: 1262-1268. PMID: 11397960, DOI: 10.1097/00007890-200105150-00014.Peer-Reviewed Original ResearchConceptsMicrovascular endothelial cellsClass II transactivatorInhibitory effectVascular diseaseSimvastatin pretreatmentIFN-gammaReductase inhibitorsClass II major histocompatibility complex moleculesCardiac transplant patientsGraft vascular diseaseLate graft failureHMG-CoA reductase inhibitorsHuman leukocyte antigenEffect of simvastatinMajor histocompatibility complex moleculesHLA-DR inductionSTAT-1 phosphorylationCoA reductase inhibitorsHistocompatibility complex moleculesHuman microvascular endothelial cellsInhibition of interferonTranscription-polymerase chain reaction analysisCardiac transplantationTransplant patientsGraft failure
2000
Simvastatin Modulates Cytokine-Mediated Endothelial Cell Adhesion Molecule Induction: Involvement of an Inhibitory G Protein
Sadeghi M, Collinge M, Pardi R, Bender J. Simvastatin Modulates Cytokine-Mediated Endothelial Cell Adhesion Molecule Induction: Involvement of an Inhibitory G Protein. The Journal Of Immunology 2000, 165: 2712-2718. PMID: 10946302, DOI: 10.4049/jimmunol.165.5.2712.Peer-Reviewed Original ResearchMeSH KeywordsAdjuvants, ImmunologicBiological TransportCell Adhesion MoleculesCells, CulturedCholesterolCytokinesDrug SynergismEndothelium, VascularE-SelectinGene Expression RegulationGTP-Binding Protein alpha Subunits, Gi-GoHumansHydroxymethylglutaryl-CoA Reductase InhibitorsIntercellular Adhesion Molecule-1Interleukin-1NF-kappa BRNA, MessengerSignal TransductionSimvastatinSodium FluorideUmbilical VeinsVascular Cell Adhesion Molecule-1ConceptsEffect of simvastatinCytokine-induced expressionIL-1Endothelial CAMsEndothelial cell adhesion molecules E-selectinNF-kappaBProinflammatory cytokines IL-1Cell adhesion molecules E-selectinAdhesion molecules E-selectinPotent immune modulatorG protein activator NaFCytokines IL-1G protein-coupled pathwayInhibitory G proteinCytokine-mediated activationSelectin mRNA levelsBasal toneProinflammatory cytokinesGialpha proteinsImmune modulatorsTNF-alphaICAM-1Pertussis toxinE-selectinEndothelial response
1999
Anchorage dependence of mitogen-induced G1 to S transition in primary T lymphocytes.
Geginat J, Bossi G, Bender J, Pardi R. Anchorage dependence of mitogen-induced G1 to S transition in primary T lymphocytes. The Journal Of Immunology 1999, 162: 5085-93. PMID: 10227977, DOI: 10.4049/jimmunol.162.9.5085.Peer-Reviewed Original ResearchMeSH KeywordsAntibodies, MonoclonalCalcium-Calmodulin-Dependent Protein KinasesCell AdhesionCell CycleCell Cycle ProteinsCell SizeCyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6Cyclin-Dependent Kinase Inhibitor p27Cyclin-Dependent KinasesDown-RegulationEnzyme ActivationG1 PhaseGene Expression RegulationGenes, fosGenes, junHumansInterleukin-2InterphaseKineticsLymphocyte Function-Associated Antigen-1Microtubule-Associated ProteinsMitogensProtein Serine-Threonine KinasesProto-Oncogene ProteinsReceptors, Antigen, T-CellS PhaseT-LymphocytesTumor Suppressor ProteinsConceptsNormal T cellsT lymphocytesT cellsPrimary T lymphocytesRetinoblastoma protein inactivationCytokines IL-2Function-blocking mAbsIL-2ICAM-1Mitogen-activated protein kinase activationCyclin-dependent kinase inhibitor p27kipIntegrins actMitogenic responseMitogenic cytokinesGrowth factorLymphocytesCell cycle progressionTCR stimulationLate componentsProtein kinase activationLeukocyte integrinsAnchorage dependenceTCR triggeringCycle progressionCellular requirements
1998
Lymphotoxin alpha3 induces chemokines and adhesion molecules: insight into the role of LT alpha in inflammation and lymphoid organ development.
Cuff C, Schwartz J, Bergman C, Russell K, Bender J, Ruddle N. Lymphotoxin alpha3 induces chemokines and adhesion molecules: insight into the role of LT alpha in inflammation and lymphoid organ development. The Journal Of Immunology 1998, 161: 6853-60. PMID: 9862717, DOI: 10.4049/jimmunol.161.12.6853.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell Adhesion MoleculesChemokine CCL2Chemokine CCL4Chemokine CCL5Chemokine CXCL10Chemokine CXCL2ChemokinesChemokines, CXCCytotoxicity, ImmunologicEmbryonic and Fetal DevelopmentE-SelectinGene Expression RegulationHumansImmunoglobulinsInflammationIntercellular Adhesion Molecule-1Lymphoid TissueLymphotoxin-alphaMacrophage Inflammatory ProteinsMiceMonokinesMucoproteinsRecombinant Fusion ProteinsSpecies SpecificityStimulation, ChemicalTumor Cells, CulturedVascular Cell Adhesion Molecule-1ConceptsLymphoid organ developmentMAdCAM-1LT-alphaLT alpha3Adhesion moleculesTreatment periodIFN-inducible protein-10Biologic activityInduction of chemokinesChemotactic protein-1Peripheral node addressinCellular adhesion moleculesMucosal addressin MAdCAM-1Unique biologic activityInflammatory mediatorsChemokine expressionProinflammatory effectsLymphoid tissueMTNF-alphaMaximal killingChemokine RANTESE-selectinKnockout miceProtein 10Alpha preparationsClass II transactivator-independent endothelial cell MHC class II gene activation induced by lymphocyte adhesion.
Collinge M, Pardi R, Bender J. Class II transactivator-independent endothelial cell MHC class II gene activation induced by lymphocyte adhesion. The Journal Of Immunology 1998, 161: 1589-93. PMID: 9712019, DOI: 10.4049/jimmunol.161.4.1589.Peer-Reviewed Original ResearchConceptsClass II transactivatorNK cellsIFN-gamma-dependent mechanismIFN-gamma-independent mannerLymphocyte adhesionMHC class II expressionHLA-DR alpha mRNAHLA-DR expressionMHC class II moleculesNK cell activationAllogeneic endothelial cellsClass II expressionIFN-gamma-induced MHC class II expressionClass II moleculesAlpha mRNA expressionCell linesHLA-DRIFN-gammaCell activationMRNA expressionEndothelial cellsAlpha mRNACellsPromoter constructsActivation
1995
Contact-dependent endothelial class II HLA gene activation induced by NK cells is mediated by IFN-gamma-dependent and -independent mechanisms.
Watson C, Petzelbauer P, Zhou J, Pardi R, Bender J. Contact-dependent endothelial class II HLA gene activation induced by NK cells is mediated by IFN-gamma-dependent and -independent mechanisms. The Journal Of Immunology 1995, 154: 3222-33. PMID: 7897208, DOI: 10.4049/jimmunol.154.7.3222.Peer-Reviewed Original ResearchMeSH KeywordsAntigens, Differentiation, B-LymphocyteBase SequenceBlotting, NorthernCell AdhesionCells, CulturedEndothelium, VascularGene Expression RegulationHistocompatibility Antigens Class IIHLA-DR AntigensHumansInterferon-gammaKiller Cells, NaturalMolecular Sequence DataOrgan Culture TechniquesPromoter Regions, GeneticSkinTranscriptional ActivationTransfectionConceptsNK cellsNK lymphocytesEndothelial cellsIFN-gammaMHC class II AgIFN-gamma dependenceT cell recruitmentClass II HLAClass II expressionHLA-DR inductionClass II AgT cell proliferationMembrane expressionTrans-well experimentsReceptor AbEndothelial activationImmune amplificationCell recruitmentMicrovessel endotheliumHuman IFN-gammaPromoter constructsClonal expansionCoculture modelCell proliferationChinese hamster ovary cells