1998
Reversal 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
1997
The 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 glomerulonephritisTNF-α Up-regulates Renal MIF Expression in Rat Crescentic Glomerulonephritis
Lan H, Yang N, Metz C, Mu W, Song Q, Nikolic-Paterson D, Bacher M, Bucala R, Atkins R. TNF-α Up-regulates Renal MIF Expression in Rat Crescentic Glomerulonephritis. Molecular Medicine 1997, 3: 136-144. PMID: 9085256, PMCID: PMC2230061, DOI: 10.1007/bf03401805.Peer-Reviewed Original ResearchConceptsRenal MIF expressionMigration inhibitory factorMIF expressionCrescentic glomerulonephritisRat crescentic glomerulonephritisMIF productionDay 1BackgroundMacrophage migration inhibitory factorSoluble TNF-α receptorTumor necrosis factor αResident kidney cellsSerum MIF levelsPotent proinflammatory mediatorPathogenesis of endotoxemiaNecrosis factor αInterstitial macrophage infiltrationTNF-α receptorExperimental crescentic glomerulonephritisMIF levelsMIF secretionRenal injuryRenal damageRenal diseaseProinflammatory mediatorsMacrophage accumulation