2000
Neurotoxicity of Advanced Glycation End-Products for Cultured Cortical Neurons
Takeuchi M, Bucala R, Suzuki T, Ohkubo T, Yamazaki M, Koike T, Kameda Y, Makita Z. Neurotoxicity of Advanced Glycation End-Products for Cultured Cortical Neurons. Journal Of Neuropathology & Experimental Neurology 2000, 59: 1094-1105. PMID: 11138929, DOI: 10.1093/jnen/59.12.1094.Peer-Reviewed Original ResearchConceptsCortical neuronsAge 2Alzheimer's diseaseEnd-stage renal diseaseNeuronal cellsAdvanced glycation end productsDM HD patientsGreater cytopathic effectsSpecific antibodiesAnti-AGE antibodyCultured cortical neuronsDose-dependent increaseGlycation end productsBlood of individualsCultured neuronal cellsDiabetes mellitusDiabetic patientsRenal diseaseNeurodegenerative processesNormal controlsAdvanced glycationCytopathic effectEpitope 1Cytotoxic effectsMTT assayImmunological Evidence that Non-carboxymethyllysine Advanced Glycation End-products Are Produced from Short Chain Sugars and Dicarbonyl Compounds in vivo
Takeuchi M, Makita Z, Bucala R, Suzuki T, Koike T, Kameda Y. Immunological Evidence that Non-carboxymethyllysine Advanced Glycation End-products Are Produced from Short Chain Sugars and Dicarbonyl Compounds in vivo. Molecular Medicine 2000, 6: 114-125. PMID: 10859028, PMCID: PMC1949938, DOI: 10.1007/bf03401779.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodiesCattleChromatography, AffinityCross ReactionsDiabetes Mellitus, Type 2Enzyme-Linked Immunosorbent AssayGlycation End Products, AdvancedGlyceraldehydeGlyoxalHumansImmunoblottingKidney Failure, ChronicLysineMaillard ReactionOxidation-ReductionPyruvaldehydeRabbitsRenal DialysisConceptsAGE antibodyCML-AGEDiabetic patientsAGE-bovine serum albuminShort Chain SugarsAdvanced glycation end productsAnti-AGE antibodyGlycation end productsAutoxidation of sugarsImmunization of rabbitsCML-BSADiabetic serumSerum albuminAdvanced glycationAGE contentSugar autoxidationRabbit serum albuminAGE modificationAntibodiesImmunological evidenceApparent molecular weightPatientsAge 3AgeImmunoblot analysis
1999
An Essential Role for Macrophage Migration Inhibitory Factor (MIF) in Angiogenesis and the Growth of a Murine Lymphoma
Chesney J, Metz C, Bacher M, Peng T, Meinhardt A, Bucala R. An Essential Role for Macrophage Migration Inhibitory Factor (MIF) in Angiogenesis and the Growth of a Murine Lymphoma. Molecular Medicine 1999, 5: 181-191. PMID: 10404515, PMCID: PMC2230298, DOI: 10.1007/bf03402061.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodiesCell DivisionCollagenDisease Models, AnimalDrug CombinationsEndothelium, VascularHumansImmunohistochemistryLamininLymphoma, B-CellMacrophage Migration-Inhibitory FactorsMiceMice, Inbred StrainsNeovascularization, PathologicOligonucleotides, AntisenseProteoglycansTumor Cells, CulturedConceptsMacrophage migration inhibitory factorRole of MIFAnti-MIF monoclonal antibodyMigration inhibitory factorB-cell lymphomaMonoclonal antibodiesCell lymphomaEffect of MIFBackgroundMacrophage migration inhibitory factorInhibitory factorC3H/HeN miceTumor-associated neovasculatureActivation of macrophagesAutocrine growth factorMicrovascular endothelial cellsCultured microvascular endothelial cellsAnti-neoplastic agentsNew blood vessel formationSolid tumor biologyEndothelial cell proliferationMIF expressionHeN miceSyngeneic modelMIF proteinTumor response
1998
Macrophage migration inhibitory factor is a critical mediator of the activation of immune cells by exotoxins of Gram-positive bacteria
Calandra T, Spiegel L, Metz C, Bucala R. Macrophage migration inhibitory factor is a critical mediator of the activation of immune cells by exotoxins of Gram-positive bacteria. Proceedings Of The National Academy Of Sciences Of The United States Of America 1998, 95: 11383-11388. PMID: 9736745, PMCID: PMC21651, DOI: 10.1073/pnas.95.19.11383.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodiesBacterial ToxinsCell DivisionCells, CulturedDisease Models, AnimalEnterotoxinsExotoxinsGram-Positive BacteriaInflammationInterferon-gammaInterleukin-2Lymphocyte ActivationMacrophage Migration-Inhibitory FactorsMacrophages, PeritonealMicePituitary GlandShock, SepticSpleenStaphylococcusStreptococcusSuperantigensConceptsMacrophage migration inhibitory factorMigration inhibitory factorMIF secretionInhibitory factorStaphylococcal toxic shock syndrome toxin 1Toxic shock syndrome toxin-1Anti-MIF antibodiesSplenocyte cytokine productionTSST-1 injectionInterferon-gamma secretionLethal mouse modelStreptococcal pyrogenic exotoxinT cell cytokinesInnate host responseLethal toxic shockProliferation of splenocytesT-cell productsInnate immune responseSyndrome toxin-1Dose-response studyMouse peritoneal macrophagesSpleen enlargementMIF antibodyC57BL/6 miceCytokine productionReversal of Established Rat Crescentic Glomerulonephritis by Blockade of Macrophage Migration Inhibitory Factor (MIF): Potential Role of MIF in Regulating Glucocorticoid Production
Yang N, Nikolic-Paterson D, Ng Y, Mu W, Metz C, Bacher M, Meinhardt A, Bucala R, Atkins R, Lan H. Reversal of Established Rat Crescentic Glomerulonephritis by Blockade of Macrophage Migration Inhibitory Factor (MIF): Potential Role of MIF in Regulating Glucocorticoid Production. Molecular Medicine 1998, 4: 413-424. PMID: 10780884, PMCID: PMC2230272, DOI: 10.1007/bf03401748.Peer-Reviewed Original ResearchConceptsMacrophage migration inhibitory factorMigration inhibitory factorCrescentic glomerulonephritisDay 7Ab treatmentRenal functionControl AbInhibitory factorPotent pro-inflammatory cytokineEndogenous glucocorticoid levelsIsotype control AbSevere renal injuryNormal renal functionCellular immune responsesPro-inflammatory cytokinesReversal of diseaseSerum corticosterone levelsExperimental crescentic glomerulonephritisInterleukin-1 productionRat crescentic glomerulonephritisCrescentic diseaseProgressive glomerulonephritisRenal injuryGBM glomerulonephritisLeukocyte infiltration