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 inhibitionMacrophagesHepatocyte Growth Factor (Hgf) Stimulates Low Density Lipoprotein Receptor-related Protein (Lrp) 5/6 Phosphorylation and Promotes Canonical Wnt Signaling*
Koraishy FM, Silva C, Mason S, Wu D, Cantley LG. Hepatocyte Growth Factor (Hgf) Stimulates Low Density Lipoprotein Receptor-related Protein (Lrp) 5/6 Phosphorylation and Promotes Canonical Wnt Signaling*. Journal Of Biological Chemistry 2014, 289: 14341-14350. PMID: 24692544, PMCID: PMC4022900, DOI: 10.1074/jbc.m114.563213.Peer-Reviewed Original ResearchConceptsΒ-catenin stabilizationRenal ischemic injuryLRP5/6 phosphorylationEpithelial cell responsesRenal proximal tubulesEpithelial cell apoptosisHepatocyte growth factorCanonical WntActive GSK3Ischemic injuryRenal epithelial cellsProximal tubulesCell responsesCanonical Wnt signalingHGF treatmentGrowth factorCell apoptosisEpithelial cellsHGFMet receptorImportant transactivatorWnt signalingInjuryLRP5/6MetS
2013
Met Activation Is Required for Early Cytoprotection after Ischemic Kidney Injury
Mason S, Hader C, Marlier A, Moeckel G, Cantley LG. Met Activation Is Required for Early Cytoprotection after Ischemic Kidney Injury. Journal Of The American Society Of Nephrology 2013, 25: 329-337. PMID: 24136921, PMCID: PMC3904569, DOI: 10.1681/asn.2013050473.Peer-Reviewed Original ResearchMeSH KeywordsAcute Kidney InjuryAnimalsApoptosisBcl-Associated Death ProteinGene Knockdown TechniquesKidneyKidney Tubules, ProximalMAP Kinase Signaling SystemMiceMice, Inbred C57BLMice, KnockoutOrgan SpecificityPhosphatidylinositol 3-KinasesPhosphorylationProtein Processing, Post-TranslationalProto-Oncogene Proteins c-aktReceptor Protein-Tyrosine KinasesReperfusion InjuryRibosomal Protein S6 Kinases, 70-kDaSignal TransductionConceptsIschemia/reperfusionKidney injuryIschemic injuryProximal tubulesInitial tubular injuryMET receptor expressionProximal tubule responseTubular cell survivalIschemic kidney injuryProximal tubule epithelial cellsRenal proximal tubule epithelial cellsTubular cell proliferationTubular cell apoptosisPI3K/Akt activationProapoptotic factor BadTubule epithelial cellsCell survivalTubule responseSerum creatinineTubular injuryKidney repairLiver abnormalitiesReceptor expressionInjuryMET activationChitinase-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
2011
Macrophages Promote Cyst Growth in Polycystic Kidney Disease
Karihaloo A, Koraishy F, Huen SC, Lee Y, Merrick D, Caplan MJ, Somlo S, Cantley LG. Macrophages Promote Cyst Growth in Polycystic Kidney Disease. Journal Of The American Society Of Nephrology 2011, 22: 1809-1814. PMID: 21921140, PMCID: PMC3187181, DOI: 10.1681/asn.2011010084.Peer-Reviewed Original ResearchConceptsPolycystic kidney diseaseCyst-lining cellsKidney diseaseCyst growthPkd1-deficient cellsContribution of inflammationMacrophage-depleted miceVehicle-treated controlsPostnatal day 10Renal functionInflammatory componentIschemic injuryOrthologous modelCre miceCystic areasLiposomal clodronateCyst progressionRenal parenchymaCystic indexTubular cellsDay 10Therapeutic potentialDay 24Macrophage migrationMacrophages
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