2007
ESDN Is a Marker of Vascular Remodeling and Regulator of Cell Proliferation in Graft Arteriosclerosis
Sadeghi MM, Esmailzadeh L, Zhang J, Guo X, Asadi A, Krassilnikova S, Fassaei HR, Luo G, Al‐Lamki R, Takahashi T, Tellides G, Bender JR, Rodriguez ER. ESDN Is a Marker of Vascular Remodeling and Regulator of Cell Proliferation in Graft Arteriosclerosis. American Journal Of Transplantation 2007, 7: 2098-2105. PMID: 17697260, DOI: 10.1111/j.1600-6143.2007.01919.x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBiomarkersCell ProliferationCells, CulturedCoronary Artery DiseaseCoronary VesselsDisease Models, AnimalHumansImmunohistochemistryMembrane ProteinsMiceMice, SCIDMuscle, Smooth, VascularReverse Transcriptase Polymerase Chain ReactionRNATissue TransplantationTransplantation, HomologousUp-RegulationConceptsGraft arteriosclerosisVascular remodelingCell proliferationSevere combined immunodeficient (SCID) miceInjury-induced vascular remodelingCombined Immunodeficient MiceHuman coronary arteriesVascular smooth muscle cell culturesVascular cell proliferationSmooth muscle cell culturesCell reconstitutionCoronary arteryImmunodeficient miceVSMC proliferationNormal arteriesArteryHuman coronaryMuscle cell culturesDiagnostic targetsHuman arteriesHigh levelsRemodelingSmooth muscle cell-derived neuropilin-like proteinArteriosclerosisProliferationActivated αvβ3 Integrin Targeting in Injury-Induced Vascular Remodeling
Sadeghi MM, Bender JR. Activated αvβ3 Integrin Targeting in Injury-Induced Vascular Remodeling. Trends In Cardiovascular Medicine 2007, 17: 5-10. PMID: 17210471, DOI: 10.1016/j.tcm.2006.07.003.Peer-Reviewed Original Research
2004
Detection of Injury-Induced Vascular Remodeling by Targeting Activated αvβ3 Integrin In Vivo
Sadeghi MM, Krassilnikova S, Zhang J, Gharaei AA, Fassaei HR, Esmailzadeh L, Kooshkabadi A, Edwards S, Yalamanchili P, Harris TD, Sinusas AJ, Zaret BL, Bender JR. Detection of Injury-Induced Vascular Remodeling by Targeting Activated αvβ3 Integrin In Vivo. Circulation 2004, 110: 84-90. PMID: 15210600, DOI: 10.1161/01.cir.0000133319.84326.70.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApolipoproteins EArterial Occlusive DiseasesCarbocyaninesCarotid StenosisCell ProliferationCells, CulturedEndothelium, VascularFemaleHeterocyclic Compounds, 1-RingHumansIntegrin alphaVbeta3MiceMice, KnockoutOrganometallic CompoundsRadioactive TracersSulfonamidesTomography, Emission-Computed, Single-PhotonConceptsCounts/pixelCarotid areaCarotid artery wire injuryEndothelial cellsIntegrin expressionInjury-induced remodelingCell proliferationDetection of injuryVascular cell proliferationCultured endothelial cellsCarotid injuryBeta3 integrin expressionWire injuryVascular proliferationRP748Vascular remodelingApolipoprotein EKi67 stainingRenal clearanceEC bindingProliferation indexSpecific radiotracersInjuryProliferative processesWeeks
2000
CD28 and LFA‐1 contribute to cyclosporin A‐resistant T cell growth by stabilizing the IL‐2 mRNA through distinct signaling pathways
Geginat J, Clissi B, Moro M, Dellabona P, Bender J, Pardi R. CD28 and LFA‐1 contribute to cyclosporin A‐resistant T cell growth by stabilizing the IL‐2 mRNA through distinct signaling pathways. European Journal Of Immunology 2000, 30: 1136-1144. PMID: 10760803, DOI: 10.1002/(sici)1521-4141(200004)30:4<1136::aid-immu1136>3.0.co;2-3.Peer-Reviewed Original ResearchMeSH KeywordsAntigens, CDB7-2 AntigenCalcineurinCD28 AntigensCells, CulturedCyclosporineCytoskeletonDendritic CellsDNA-Binding ProteinsDrug SynergismHumansIntercellular Adhesion Molecule-1Interleukin-2Lymphocyte ActivationLymphocyte Function-Associated Antigen-1Membrane GlycoproteinsMitogen-Activated Protein KinasesNF-kappa BNFATC Transcription FactorsNuclear ProteinsPromoter Regions, GeneticProtein BindingRNA StabilityRNA, MessengerSignal TransductionSuperantigensT-LymphocytesTranscription FactorsConceptsIL-2 mRNALFA-1ICAM-1IL-2 dependentT cell proliferationSubsequent T cell proliferationCostimulatory molecule CD28TCR-induced proliferationSignaling pathwaysT cell growthIL-2 transcriptsGraft rejectionDendritic cellsIL-2Clinical transplantationT lymphocytesMolecule CD28Primary T lymphocytesNF-kappaBCD28Distinct signaling pathwaysLower transcriptional rateDifferent signaling pathwaysProtein kinase activationCell proliferation
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