2019
Tubular GM-CSF Promotes Late MCP-1/CCR2-Mediated Fibrosis and Inflammation after Ischemia/Reperfusion Injury
Xu L, Sharkey D, Cantley LG. Tubular GM-CSF Promotes Late MCP-1/CCR2-Mediated Fibrosis and Inflammation after Ischemia/Reperfusion Injury. Journal Of The American Society Of Nephrology 2019, 30: 1825-1840. PMID: 31315923, PMCID: PMC6779361, DOI: 10.1681/asn.2019010068.Peer-Reviewed Original ResearchConceptsIschemia/reperfusion injuryWild-type miceTubular cellsTubular injuryReperfusion injuryImmune cellsKidney ischemia/reperfusion injuryUnilateral ischemia/reperfusion injuryMCP-1/CCR2Monocyte chemoattractant protein-1Initial kidney damageInjured tubular cellsKidney 14 daysKidney injury markersProgressive interstitial fibrosisProfibrotic growth factorsChemoattractant protein-1MCP-1 receptorGranulocyte-macrophage colony-stimulating factorRenal tubular cellsNumber of macrophagesTime of repairColony-stimulating factorCoculture of macrophagesMacrophages persist
2014
GM-CSF Promotes Macrophage Alternative Activation after Renal Ischemia/Reperfusion Injury
Huen SC, Huynh L, Marlier A, Lee Y, Moeckel GW, Cantley LG. GM-CSF Promotes Macrophage Alternative Activation after Renal Ischemia/Reperfusion Injury. Journal Of The American Society Of Nephrology 2014, 26: 1334-1345. PMID: 25388222, PMCID: PMC4446881, DOI: 10.1681/asn.2014060612.Peer-Reviewed Original ResearchMeSH KeywordsAcute Kidney InjuryAnalysis of VarianceAnimalsBlotting, WesternCell ProliferationCells, CulturedDisease Models, AnimalGene Expression RegulationGranulocyte-Macrophage Colony-Stimulating FactorImmunohistochemistryKidney Tubules, ProximalMacrophage ActivationMaleMiceMice, Inbred C57BLMultivariate AnalysisPhenotypeRandom AllocationReal-Time Polymerase Chain ReactionReperfusion InjurySignal TransductionUp-RegulationConceptsIschemia/reperfusion injuryMacrophage alternative activationBone marrow-derived macrophagesAlternative activationMarrow-derived macrophagesTubular cellsGM-CSFReperfusion injuryReparative phenotypeTubular proliferationKidney ischemia/reperfusion injuryRenal ischemia/reperfusion injuryMouse proximal tubule cellsInitial kidney damageRepair phaseProximal tubule cellsTubular factorsIschemic injuryKidney damageProinflammatory macrophagesRenal repairMacrophage activationTubule cellsPharmacologic inhibitionMacrophages
2013
Chitinase-Like Protein Brp-39/YKL-40 Modulates the Renal Response to Ischemic Injury and Predicts Delayed Allograft Function
Schmidt IM, Hall IE, Kale S, Lee S, He CH, Lee Y, Chupp GL, Moeckel GW, Lee CG, Elias JA, Parikh CR, Cantley LG. Chitinase-Like Protein Brp-39/YKL-40 Modulates the Renal Response to Ischemic Injury and Predicts Delayed Allograft Function. Journal Of The American Society Of Nephrology 2013, 24: 309-319. PMID: 23291472, PMCID: PMC3559482, DOI: 10.1681/asn.2012060579.Peer-Reviewed Original ResearchMeSH KeywordsAdipokinesAnimalsApoptosisBiomarkersCells, CulturedChitinase-3-Like Protein 1Delayed Graft FunctionDisease Models, AnimalEpithelial CellsGlycoproteinsHumansKidneyKidney TransplantationLectinsMacrophagesMaleMiceMice, Inbred C57BLPhosphatidylinositol 3-KinasesPredictive Value of TestsProto-Oncogene Proteins c-aktReperfusion InjurySignal TransductionTransplantation, HomologousConceptsBRP-39/YKLGraft functionKidney injuryYKL-40Reparative responseDeceased donor kidney transplantationKidney ischemia/reperfusionHours of transplantImmediate graft functionDelayed graft functionTubular cell deathIschemia/reperfusionDegree of injuryAllograft functionCell apoptotic deathKidney hypoperfusionKidney transplantationSystemic hypotensionRenal failureIschemic injuryRenal ischemiaRenal responseUrinary levelsBRP-39Activation of Akt
1997
Modulation of c-fos and egr-1 expression in the isolated perfused kidney by agents that alter tubular work
Joannidis M, Cantley L, Spokes K, Stuart-Tilley A, Alper S, Epstein F. Modulation of c-fos and egr-1 expression in the isolated perfused kidney by agents that alter tubular work. Kidney International 1997, 52: 130-139. PMID: 9211355, DOI: 10.1038/ki.1997.312.Peer-Reviewed Original ResearchMeSH KeywordsAmino AcidsAnimalsBlotting, NorthernCell HypoxiaCells, CulturedDNA-Binding ProteinsDogsEarly Growth Response Protein 1Fluorescent Antibody Technique, IndirectGene Expression RegulationGlycineImmediate-Early ProteinsImmunohistochemistryIn Vitro TechniquesKidneyMaleOuabainProto-Oncogene Proteins c-fosRatsRats, Sprague-DawleyTime FactorsTranscription FactorsConceptsMedullary thick ascending limbThick ascending limbHypoxic injuryOuter medullaStandard perfusionC-fosMRNA levelsIEG expressionAscending limbEgr-1Immediate early gene c-fosAbsence of reperfusionEarly gene c-fosKrebs-Henseleit bufferGene c-fosImmediate early gene expressionInhibition of NaEgr-1 expressionHypoxic damageRenal cortexImmunohistochemical demonstrationRenal epithelial cellsTubular transportCultured renal epithelial cellsIEG mRNA levels
1993
Effects of Ioversol versus Iothalamate on Endothelin Release and Radiocontrast Nephropathy
HEYMAN S, CLARK B, CANTLEY L, SPOKES K, ROSEN S, BREZIS M, EPSTEIN F. Effects of Ioversol versus Iothalamate on Endothelin Release and Radiocontrast Nephropathy. Investigative Radiology 1993, 28: 313-318. PMID: 8478171, DOI: 10.1097/00004424-199304000-00011.Peer-Reviewed Original ResearchConceptsEffects of ioversolEndothelin releaseRadiocontrast nephropathyRadiocontrast agentsEqui-iodine dosesRelease of endothelinLow-osmolar agentsCultured bovine aortic endothelial cellsAortic endothelial cellsRenal vasoconstrictionBovine aortic endothelial cellsRenal vasoconstrictorCreatinine clearanceRenal functionOsmolar agentsRenal toxicityMorphologic damageNormal ratsVascular endotheliumSalt depletionNephropathyRenal medullaRatsEndothelial cellsIoversol