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
2001
Macrophage 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
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 nephritis
1997
Insulin secretion is regulated by the glucose-dependent production of islet β cell macrophage migration inhibitory factor
Waeber G, Calandra T, Roduit R, Haefliger J, Bonny C, Thompson N, Thorens B, Temler E, Meinhardt A, Bacher M, Metz C, Nicod P, Bucala R. Insulin secretion is regulated by the glucose-dependent production of islet β cell macrophage migration inhibitory factor. Proceedings Of The National Academy Of Sciences Of The United States Of America 1997, 94: 4782-4787. PMID: 9114069, PMCID: PMC20802, DOI: 10.1073/pnas.94.9.4782.Peer-Reviewed Original ResearchConceptsMacrophage migration inhibitory factorMigration inhibitory factorInsulin releaseInsulin secretionBeta cellsRecombinant macrophage migration inhibitory factorInhibitory factorGlucose-induced insulin releasePancreatic islet beta cellsInsulin-secreting beta cellsINS-1 cell lineIslet beta cellsIsolated rat isletsInsulin secretion responseIslets of LangerhansConcentration-dependent mannerIslet cell productsImmune cellsT lymphocytesPituitary hormonesPerifusion studiesAutocrine fashionRat isletsSecretion responseGlucocorticoid stimulationThe Pathogenic Role of Macrophage Migration Inhibitory Factor in Immunologically Induced Kidney Disease in the Rat
Lan H, Bacher M, Yang N, Mu W, Nikolic-Paterson D, Metz C, Meinhardt A, Bucala R, Atkins R. The Pathogenic Role of Macrophage Migration Inhibitory Factor in Immunologically Induced Kidney Disease in the Rat. Journal Of Experimental Medicine 1997, 185: 1455-1466. PMID: 9126926, PMCID: PMC2196273, DOI: 10.1084/jem.185.8.1455.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, MonoclonalAntibody FormationCell Adhesion MoleculesGene ExpressionGlomerulonephritisHypersensitivity, DelayedIntercellular Adhesion Molecule-1Interleukin-1Macrophage Migration-Inhibitory FactorsMaleMiceNitric Oxide SynthaseRabbitsRatsRats, Sprague-DawleyRNA, MessengerSkinTime FactorsVascular Cell Adhesion Molecule-1ConceptsMacrophage migration inhibitory factorControl antibody-treated animalsDelayed-type hypersensitivity responseAnti-MIF treatmentAntibody-treated animalsMigration inhibitory factorAdhesion molecule-1Hypersensitivity responseKidney diseaseLeukocytic infiltrationHistological damageCrescentic anti-glomerular basement membrane (GBM) glomerulonephritisMolecule-1Skin delayed-type hypersensitivity responseInducible nitric oxide synthase (iNOS) expressionAnti-glomerular basement membrane glomerulonephritisInhibitory factorVascular cell adhesion molecule-1Nitric oxide synthase expressionIntercellular adhesion molecule-1Cell adhesion molecule-1Rabbit anti-rat GBM serumProgressive renal injuryRenal function impairmentAnti-GBM glomerulonephritis
1994
Differential expression of the small inducible cytokines GRO α and GROβ by synovial fibroblasts in chronic arthritis: Possible role in growth regulation
Hogan M, Sherry B, Ritchlin C, Fabre M, Winchester R, Cerami A, Bucala R. Differential expression of the small inducible cytokines GRO α and GROβ by synovial fibroblasts in chronic arthritis: Possible role in growth regulation. Cytokine 1994, 6: 61-69. PMID: 8003635, DOI: 10.1016/1043-4666(94)90009-4.Peer-Reviewed Original ResearchMeSH KeywordsActinsArthritis, RheumatoidBase SequenceCells, CulturedChemokine CXCL1Chemokines, CXCChemotactic FactorsConsensus SequenceCytokinesDNA PrimersFibroblastsGene ExpressionGrowth SubstancesHumansIntercellular Signaling Peptides and ProteinsInterleukin-8Molecular Sequence DataPolymerase Chain ReactionRNA, MessengerSulfur RadioisotopesSynovial MembraneTranscription, GeneticConceptsSynovial fibroblastsGRO alphaChronic arthritisRheumatoid synoviaSynovial fibroblast cell lineGRO betaPro-inflammatory statePro-inflammatory activityRheumatoid arthritisChronic inflammationConnective tissue responseRheumatoid synoviumInflammatory cytokinesRate of proliferationSynovial pannusCytokine activationGRO gammaMetalloproteinase activityArthritisSynoviaGrowth factorConstitutive expressionGrowth dysregulationTissue responseCell lines