2024
Prognostic and therapeutic insights into MIF, DDT, and CD74 in melanoma
Valdez C, Sánchez-Zuno G, Osmani L, Ibrahim W, Galan A, Bacchiocchi A, Halaban R, Kulkarni R, Kang I, Bucala R, Tran T. Prognostic and therapeutic insights into MIF, DDT, and CD74 in melanoma. Oncotarget 2024, 15: 507-520. PMID: 39028303, PMCID: PMC11259151, DOI: 10.18632/oncotarget.28615.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAntigens, Differentiation, B-LymphocyteBiomarkers, TumorFemaleHistocompatibility Antigens Class IIHumansImmune Checkpoint InhibitorsIntramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsMaleMelanomaMiddle AgedMutationPrognosisRetrospective StudiesSkin NeoplasmsConceptsMacrophage migration inhibitory factorImmune checkpoint inhibitionD-dopachrome tautomeraseExpression of macrophage migration inhibitory factorDrivers of tumor progressionInflammatory cell markersPatient tumor samplesPatient survival outcomesMigration inhibitory factorStatistically significant differenceCheckpoint inhibitionImmune therapyPrognostic valueSurvival outcomesResistant melanomaGene expressionImproved survivalRetrospective studyInflammatory markersTumor progressionCell markersTumor samplesClinical evidenceMelanomaBulk RNA sequencingDownregulation of adipose LPL by PAR2 contributes to the development of hypertriglyceridemia
Huang Y, Chen L, Li L, Qi Y, Tong H, Wu H, Xu J, Leng L, Cheema S, Sun G, Xia Z, McGuire J, Rodrigues B, Young L, Bucala R, Qi D. Downregulation of adipose LPL by PAR2 contributes to the development of hypertriglyceridemia. JCI Insight 2024, 9: e173240. PMID: 38973609, PMCID: PMC11383372, DOI: 10.1172/jci.insight.173240.Peer-Reviewed Original ResearchConceptsMacrophage migration inhibitory factorDevelopment of hypertriglyceridemiaWhite adipose tissueAdipose LPLPAR2 expressionLevels of macrophage migration inhibitory factorElevated plasma TG levelsLPL expressionLipoprotein lipaseIncrease PAR2 expressionPlasma MIF levelsPlasma TG levelsMigration inhibitory factorPalmitic acid dietInhibited Akt phosphorylationMIF levelsLipoprotein lipase geneTG levelsObese humansPlasma TGHypertriglyceridemiaAkt phosphorylationLipid storageInhibitory factorAdipose tissue
2022
CD74 ablation rescues type 2 diabetes mellitus-induced cardiac remodeling and contractile dysfunction through pyroptosis-evoked regulation of ferroptosis
Chen L, Yin Z, Qin X, Zhu X, Chen X, Ding G, Sun D, Wu NN, Fei J, Bi Y, Zhang J, Bucala R, Ren J, Zheng Q. CD74 ablation rescues type 2 diabetes mellitus-induced cardiac remodeling and contractile dysfunction through pyroptosis-evoked regulation of ferroptosis. Pharmacological Research 2022, 176: 106086. PMID: 35033649, DOI: 10.1016/j.phrs.2022.106086.Peer-Reviewed Original ResearchMeSH KeywordsAdultAnimalsAntigens, Differentiation, B-LymphocyteCell LineDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2FemaleFerroptosisGene ExpressionHistocompatibility Antigens Class IIHumansMacrophage Migration-Inhibitory FactorsMaleMice, KnockoutMiddle AgedMyocardial ContractionMyocardiumNLR Family, Pyrin Domain-Containing 3 ProteinOxidative StressOxygen ConsumptionPyroptosisRatsVentricular RemodelingConceptsHigh glucose/high fatMacrophage migration inhibitory factorCardiac remodelingContractile dysfunctionCell death domainGene Ontology termsInhibitors of MIFRecombinant macrophage migration inhibitory factorCytokine macrophage migration inhibitory factorType 2 diabetes mellitusOntology termsDeath domainLipid peroxidationGlobal metabolic defectsKEGG analysisPlasma MIF levelsInjection of streptozotocinMitochondrial defectsHigh-fat dietMigration inhibitory factorInhibitor of NLRP3Cell deathPrecise interplayMitochondrial dysfunctionCognate receptors
2020
Designed CXCR4 mimic acts as a soluble chemokine receptor that blocks atherogenic inflammation by agonist-specific targeting
Kontos C, El Bounkari O, Krammer C, Sinitski D, Hille K, Zan C, Yan G, Wang S, Gao Y, Brandhofer M, Megens RTA, Hoffmann A, Pauli J, Asare Y, Gerra S, Bourilhon P, Leng L, Eckstein HH, Kempf WE, Pelisek J, Gokce O, Maegdefessel L, Bucala R, Dichgans M, Weber C, Kapurniotu A, Bernhagen J. Designed CXCR4 mimic acts as a soluble chemokine receptor that blocks atherogenic inflammation by agonist-specific targeting. Nature Communications 2020, 11: 5981. PMID: 33239628, PMCID: PMC7689490, DOI: 10.1038/s41467-020-19764-z.Peer-Reviewed Original ResearchMeSH KeywordsAgedAnimalsAntigens, CDAtherosclerosisBinding SitesCarotid Artery, CommonChemokine CXCL12Crystallography, X-RayDisease Models, AnimalDrug DesignDrug Evaluation, PreclinicalEndarterectomy, CarotidFemaleHumansIntramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsMaleMiceMice, Knockout, ApoEMiddle AgedPeptide FragmentsReceptors, CXCR4SialyltransferasesSignal TransductionConceptsMacrophage migration inhibitory factorCXC motif chemokine receptor 4Chemokine receptorsChemokine/receptor axisCXCR4/CXCL12 interactionHuman carotid endarterectomy specimensMigration inhibitory factorChemokine receptor 4MIF/CD74Carotid endarterectomy specimensAtherogenic inflammationCXCL12 interactionReceptor axisReceptor 4MIF inhibitorsReceptor-based strategiesAtherosclerotic plaquesAtherosclerosisAtypical chemokineLeukocyte adhesionCell activityProtective pathwaysInflammationChemokinesPlaques
2001
Lysozyme Enhances Renal Excretion of Advanced Glycation Endproducts In Vivo and Suppresses Adverse AGE-mediated Cellular Effects In Vitro: A Potential AGE Sequestration Therapy for Diabetic Nephropathy?
Zheng F, Cai W, Mitsuhashi T, Vlassara H, Bucala R. Lysozyme Enhances Renal Excretion of Advanced Glycation Endproducts In Vivo and Suppresses Adverse AGE-mediated Cellular Effects In Vitro: A Potential AGE Sequestration Therapy for Diabetic Nephropathy? Molecular Medicine 2001, 7: 737-747. PMID: 11788787, PMCID: PMC1950004, DOI: 10.1007/bf03401963.Peer-Reviewed Original ResearchConceptsAdvanced glycation endproductsSerum advanced glycation endproductsDb/db miceNon-obese diabeticSerum AGEsMesangial cellsDb miceAGE-BSAGlycation endproductsIGF-I productionDiabetic renal damageSprague-Dawley ratsAGE clearanceSuppress macrophagesNOD miceDiabetic nephropathyRenal damageRenal excretionNormal ratsMMP-9Type IV collagenHost defense proteinsExcretionMRNA levelsMiceURINE MACROPHAGE MIGRATION INHIBITORY FACTOR CONCENTRATIONS AS A DIAGNOSTIC TOOL IN HUMAN RENAL ALLOGRAFT REJECTION1
Brown F, Nikolic-Paterson D, Chadban S, Dowling J, Jose M, Metz C, Bucala R, Atkins R. URINE MACROPHAGE MIGRATION INHIBITORY FACTOR CONCENTRATIONS AS A DIAGNOSTIC TOOL IN HUMAN RENAL ALLOGRAFT REJECTION1. Transplantation 2001, 71: 1777-1783. PMID: 11455258, DOI: 10.1097/00007890-200106270-00013.Peer-Reviewed Original ResearchConceptsMacrophage migration inhibitory factorAcute rejectionMIF concentrationsRenal transplant patientsCyA toxicityTransplant patientsProspective studyRetrospective studyNormal controlsSerum macrophage migration inhibitory factorUrine macrophage migration inhibitory factorAcute renal allograft rejectionStable renal transplant patientsDay 1 posttransplantationEpisodes of biopsyLocal MIF productionRenal allograft patientsRENAL ALLOGRAFT REJECTION1Renal transplant dysfunctionSerum MIF concentrationsSerum MIF levelsTransplant patient groupsRenal allograft rejectionPro-inflammatory cytokinesNormal healthy controls
2000
Expression of macrophage migration inhibitory factor in human glomerulonephritis
Lan H, Yang N, Nikolic-Paterson D, Yu X, Mu W, Isbel N, Metz C, Bucala R, Atkins R. Expression of macrophage migration inhibitory factor in human glomerulonephritis. Kidney International 2000, 57: 499-509. PMID: 10652026, DOI: 10.1046/j.1523-1755.2000.00869.x.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAgedAged, 80 and overBiopsyCohort StudiesEpithelial CellsFemaleGene ExpressionGlomerulonephritis, MembranoproliferativeGlomerulonephritis, MembranousHumansIn Situ HybridizationKidney GlomerulusMacrophage Migration-Inhibitory FactorsMacrophagesMaleMiddle AgedReference ValuesRNA, MessengerT-LymphocytesConceptsMacrophage migration inhibitory factorMIF expressionMigration inhibitory factorFocal segmental glomerulosclerosisHuman glomerulonephritisProliferative formsMIF mRNAPathogenic roleExperimental glomerulonephritisInhibitory factorProgressive formRenal MIF expressionRenal function impairmentT cell accumulationT-cell infiltratesEpithelial cellsMinimal change diseaseFocal segmental lesionsGlomerular endothelial cellsTubular epithelial cellsNormal human kidneyAttractive therapeutic targetCreatinine clearanceGlomerular epithelial cellsLupus nephritisProtection from septic shock by neutralization of macrophage migration inhibitory factor
Calandra T, Echtenacher B, Roy D, Pugin J, Metz C, Hültner L, Heumann D, Männel D, Bucala R, Glauser M. Protection from septic shock by neutralization of macrophage migration inhibitory factor. Nature Medicine 2000, 6: 164-170. PMID: 10655104, DOI: 10.1038/72262.Peer-Reviewed Original ResearchConceptsMacrophage migration inhibitory factorSeptic shockMigration inhibitory factorLethal peritonitisSevere sepsisMIF antibodyRecombinant macrophage migration inhibitory factorAnti-tumor necrosis factorInhibitory factorTNFα knockout micePathogenesis of sepsisPlasma of patientsNew therapeutic targetsBacterial peritonitisIll patientsInvestigational therapiesCecal ligationNecrosis factorNormal micePivotal cytokineSystemic circulationKnockout miceTherapeutic targetSepsisPeritonitis
1997
Reduction of plasma apolipoprotein-B by effective removal of circulating glycation derivatives in uremia
Fishbane S, Bucala R, Pereira B, Founds H, Vlassara H. Reduction of plasma apolipoprotein-B by effective removal of circulating glycation derivatives in uremia. Kidney International 1997, 52: 1645-1650. PMID: 9407512, DOI: 10.1038/ki.1997.497.Peer-Reviewed Original ResearchConceptsAdvanced glycation endoproductsLow density lipoprotein clearanceLong-term hemodialysis therapyRenal replacement treatmentEffect of hemodialysisAGE removalDiabetic ESRDSerum apoBESRD patientsRenal insufficiencyClinical outcomesLipoprotein clearancePlasma apoBHemodialysis therapyReplacement treatmentApoliprotein BPatientsGroup subjectsHemodialysis filtersReactive substancesApoBPlasma apolipoproteinsAGE clearanceBaselineClearanceElevated AGE-Modified ApoB in Sera of Euglycemic, Normolipidemic Patients with Atherosclerosis: Relationship to Tissue AGEs
Stitt A, He C, Friedman S, Scher L, Rossi P, Ong L, Founds H, Li Y, Bucala R, Vlassara H. Elevated AGE-Modified ApoB in Sera of Euglycemic, Normolipidemic Patients with Atherosclerosis: Relationship to Tissue AGEs. Molecular Medicine 1997, 3: 617-627. PMID: 9323713, PMCID: PMC2230092, DOI: 10.1007/bf03401819.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAgingApolipoproteins BArteriosclerosisCarotid ArteriesCollagenEndothelium, VascularEnzyme-Linked Immunosorbent AssayFemaleGlycation End Products, AdvancedHumansImmunohistochemistryMacrophagesMaleMicroscopy, FluorescenceMiddle AgedReceptor for Advanced Glycation End ProductsReceptors, ImmunologicRegression AnalysisConceptsSmooth muscle cellsAGE-specific receptorsMononuclear cellsAtherosclerotic vascular diseaseOcclusive atherosclerotic diseaseDevelopment of hyperlipidemiaLipid-laden macrophagesYoung healthy personsEarly-stage lesionsCardiac bypass patientsAGE-R1Nondiabetic patientsAsymptomatic patientsAsymptomatic personsBypass patientsNormolipidemic patientsAtherosclerotic diseaseDistribution of ageVascular diseaseInflammatory responseLate-stage plaquesAtheromatous lesionsEarly lesionsFatty streaksNondiabetic etiologyOrally absorbed reactive glycation products (glycotoxins): An environmental risk factor in diabetic nephropathy
Koschinsky T, He C, Mitsuhashi T, Bucala R, Liu C, Buenting C, Heitmann K, Vlassara H. Orally absorbed reactive glycation products (glycotoxins): An environmental risk factor in diabetic nephropathy. Proceedings Of The National Academy Of Sciences Of The United States Of America 1997, 94: 6474-6479. PMID: 9177242, PMCID: PMC21074, DOI: 10.1073/pnas.94.12.6474.Peer-Reviewed Original ResearchConceptsAdvanced glycation endproductsDietary advanced glycation endproductsEndogenous advanced glycation endproductsDiabetes mellitusKidney diseaseRenal excretionRenal vascular injuryDiabetic nephropathy patientsSerum AGE levelsDegree of albuminuriaNondiabetic kidney diseaseEnvironmental risk factorsAGE immunoreactivityRenal complicationsCreatinine clearanceDiabetic nephropathyNephropathy patientsRenal failureDiabetic patientsRisk factorsFood intakeHealthy subjectsGlycation endproductsDietary restrictionCL diet
1996
Glycation and microglial reaction in lesions of Alzheimer's disease
Dickson D, Sinicropi S, Yen S, Ko L, Mattiace L, Bucala R, Vlassara H. Glycation and microglial reaction in lesions of Alzheimer's disease. Neurobiology Of Aging 1996, 17: 733-743. PMID: 8892346, DOI: 10.1016/0197-4580(96)00116-9.Peer-Reviewed Original ResearchConceptsAdvanced glycation end productsAGE immunoreactivityNeurofibrillary tanglesExtracellular neurofibrillary tanglesAmyloid depositsMicroglial reactionActivation of microgliaIntracellular neurofibrillary tanglesAlzheimer's disease brainPattern of immunoreactivityGlycation end productsTriple immunostainingDisease brainSenile plaquesDiffuse amyloidAlzheimer's diseaseImmunoreactivityCryostat sectionsDouble labelingAntibodiesMicrogliaLesionsPolyclonal antibodiesDiseaseGlycation
1995
Formation of Immunochemical Advanced Glycosylation End Products Precedes and Correlates With Early Manifestations of Renal and Retinal Disease in Diabetes
Beisswenger P, Makita Z, Curphey T, Moore L, Jean S, Brinck-Johnsen T, Bucala R, Vlassara H. Formation of Immunochemical Advanced Glycosylation End Products Precedes and Correlates With Early Manifestations of Renal and Retinal Disease in Diabetes. Diabetes 1995, 44: 824-829. PMID: 7789650, DOI: 10.2337/diab.44.7.824.Peer-Reviewed Original ResearchConceptsAdvanced glycosylation end productsEnzyme-linked immunosorbent assayAlbumin excretionDuration of diabetesElevated levelsNormal renal statusTissue advanced glycosylation end productsDiabetic vascular complicationsTissue AGE levelsGlycosylation end productsEvident retinopathyMicroalbuminuric phaseOvert microangiopathySevere retinopathyVascular complicationsDiabetic nephropathyRenal statusUrinary albuminProliferative retinopathyEarly retinopathyHigher age levelsSignificant elevationRetinopathyRetinal diseasesEarly manifestationImmunohistochemical detection of advanced glycosylation end products within the vascular lesions and glomeruli in diabetic nephropathy
Nishino T, Horii Y, Shiiki H, Yamamoto H, Makita Z, Bucala R, Dohi K. Immunohistochemical detection of advanced glycosylation end products within the vascular lesions and glomeruli in diabetic nephropathy. Human Pathology 1995, 26: 308-313. PMID: 7890283, DOI: 10.1016/0046-8177(95)90063-2.Peer-Reviewed Original ResearchConceptsAdvanced glycosylation end productsGlycosylation end productsSevere diffuse lesionsAnti-AGE antibodyComplications of diabetesInner elastic layerRenal complicationsDiabetic nephropathyAGE antibodyDiffuse lesionsNondiabetic individualsVascular lesionsPathogenic roleAGE accumulationHyaline depositsImmunohistochemical stainingPositive stainingImmunohistochemical detectionAdvanced glycosylationVascular intimaNormal agingSpecific antibodiesTissue distributionEnd productsAntibodies
1992
Hemoglobin-AGE: A Circulating Marker of Advanced Glycosylation
Makita Z, Vlassara H, Rayfield E, Cartwright K, Friedman E, Rodby R, Cerami A, Bucala R. Hemoglobin-AGE: A Circulating Marker of Advanced Glycosylation. Science 1992, 258: 651-653. PMID: 1411574, DOI: 10.1126/science.1411574.Peer-Reviewed Original ResearchConceptsAdvanced glycosylation end productsAdvanced glycosylationAGE-modified formAGE-specific antibodiesComplications of agingDiabetes-induced hyperglycemiaAge-related complicationsGlycosylation end productsCirculating MarkersDiabetic patientsRenal diseaseGlucose-derived Amadori productsNormal individualsComplicationsPatientsTissue modificationsTissue proteinsHemoglobinAmadori productsEnd productsPercentDiabeticsHyperglycemiaAtherosclerosisDiabetes
1985
Determination of 16 alpha‐hydroxyestrone by radioimmunoassay in systemic lupus erythematosus
Lahita R, Bucala R, Bradlow H, Fishman J. Determination of 16 alpha‐hydroxyestrone by radioimmunoassay in systemic lupus erythematosus. Arthritis & Rheumatism 1985, 28: 1122-1127. PMID: 4052123, DOI: 10.1002/art.1780281007.Peer-Reviewed Original ResearchConceptsSystemic lupus erythematosusActive diseaseLupus erythematosusInactive systemic lupus erythematosusVariety of seraInactive diseaseSLE patientsAntibody levelsComplement levelsRheumatic diseasesLaboratory criteriaAlpha-hydroxyestroneHormone levelsHealthy volunteersNormal controlsPatientsEstrogenic metabolitesNormal levelsDiseaseErythematosusSignificant increaseRadioimmunoassayPoor correlationMetabolitesHigh levelsIncreased Levels of 16α-Hydroxyestrone-Modified Proteins in Pregnancy and in Systemic Lupus Erythematosus*
BUCALA R, LAHITA R, FISHMAN J, CERAMI A. Increased Levels of 16α-Hydroxyestrone-Modified Proteins in Pregnancy and in Systemic Lupus Erythematosus*. The Journal Of Clinical Endocrinology & Metabolism 1985, 60: 841-847. PMID: 3920233, DOI: 10.1210/jcem-60-5-841.Peer-Reviewed Original ResearchConceptsSystemic lupus erythematosusLupus erythematosusPregnant womenHigher mean levelsNormal womenAlpha-hydroxyestroneFemale hormonesNormal subjectsErythematosusNormal levelsElevated levelsMean levelsWomenLatter groupRed cellsLymphocyte proteinSimilar elevationsPregnancyOHEBasement membrane proteinsUseful indicatorLevelsPatientsModification of proteinsLymphocytes