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
The Terminator mouse is a diphtheria toxin–receptor knock-in mouse strain for rapid and efficient enrichment of desired cell lineages
Guo JK, Shi H, Koraishy F, Marlier A, Ding Z, Shan A, Cantley LG. The Terminator mouse is a diphtheria toxin–receptor knock-in mouse strain for rapid and efficient enrichment of desired cell lineages. Kidney International 2013, 84: 1041-1046. PMID: 23739236, PMCID: PMC3775868, DOI: 10.1038/ki.2013.202.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBiomarkersBlotting, WesternCell LineageCell SeparationCell SurvivalDiphtheria ToxinGenotypeHeparin-binding EGF-like Growth FactorImmunohistochemistryIntegrasesIntercellular Signaling Peptides and ProteinsKidney Tubules, ProximalMiceMice, Inbred C57BLMice, TransgenicPhenotypePodocytesPrimary Cell CultureRNA, UntranslatedTime FactorsConceptsDiphtheria toxin treatmentToxin treatmentPrimary culturesDiphtheria toxin receptor expressionDiphtheria toxin receptorCell typesProximal tubule cellsPodocin-cre miceToxin exposureTubule cellsMiceMouse strainsWestern blottingToxin receptorKidney cellsSpecific cell typesMarker proteinsCell lineagesCellsTreatment
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
1995
Induction of heat-shock proteins does not prevent renal tubular injury following ischemia
Joannidis M, Cantley L, Spokes K, Medina R, Pullman J, Rosen S, Epstein F. Induction of heat-shock proteins does not prevent renal tubular injury following ischemia. Kidney International 1995, 47: 1752-1759. PMID: 7643546, DOI: 10.1038/ki.1995.242.Peer-Reviewed Original ResearchConceptsHeat shock proteinsMedullary hypoxic injuryPossible protective effectRenal tubular injuryDifferent experimental modelsSevere morphological damageSerum creatinineTubular injuryCross clampingIschemic injuryRight kidneyRenal arteryHypoxic injuryControl ratsIntact ratsRenal cortexProtective effectImmunohistochemical meansUrea nitrogenProximal tubulesHeat shockRenal cellsRat kidneyKidneyMorphological damage