2022
Authors' Reply: Most Arginase-1 Positive Cells Are Likely Injured S3 Proximal Tubular Cells Carrying Upregulated Phagocytotic Capacity rather than M2 Macrophages—Too Many To Be True
Shin N, Marlier A, Xu L, Doilicho N, Linberg D, Guo J, Cantley L. Authors' Reply: Most Arginase-1 Positive Cells Are Likely Injured S3 Proximal Tubular Cells Carrying Upregulated Phagocytotic Capacity rather than M2 Macrophages—Too Many To Be True. Journal Of The American Society Of Nephrology 2022, 33: 2124-2125. PMID: 36316094, PMCID: PMC9678031, DOI: 10.1681/asn.2022070836.Peer-Reviewed Original ResearchArginase-1 Is Required for Macrophage-Mediated Renal Tubule Regeneration
Shin NS, Marlier A, Xu L, Doilicho N, Linberg D, Guo J, Cantley LG. Arginase-1 Is Required for Macrophage-Mediated Renal Tubule Regeneration. Journal Of The American Society Of Nephrology 2022, 33: 1077-1086. PMID: 35577558, PMCID: PMC9161787, DOI: 10.1681/asn.2021121548.Peer-Reviewed Original ResearchConceptsIschemia-reperfusion injuryTubular cell proliferationArginase-1Contralateral nephrectomyRenal repairFl/Littermate controlsTubular cellsReceptor 1GM-CSFRenal tubular cell proliferationRenal tubule regenerationMacrophage scavenger receptor 1Mannose receptor 1Cell proliferative responsesCell proliferationScavenger receptor 1Coculture of macrophagesDead cell debrisKidney injuryKidney repairRenal responseProinflammatory activationTubule regenerationMouse survival
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
2018
Mcp1 Promotes Macrophage-Dependent Cyst Expansion in Autosomal Dominant Polycystic Kidney Disease
Cassini MF, Kakade VR, Kurtz E, Sulkowski P, Glazer P, Torres R, Somlo S, Cantley LG. Mcp1 Promotes Macrophage-Dependent Cyst Expansion in Autosomal Dominant Polycystic Kidney Disease. Journal Of The American Society Of Nephrology 2018, 29: 2471-2481. PMID: 30209078, PMCID: PMC6171277, DOI: 10.1681/asn.2018050518.Peer-Reviewed Original ResearchConceptsAutosomal dominant polycystic kidney diseaseSingle knockout miceTubular cell injuryDominant polycystic kidney diseaseCyst growthPolycystic kidney diseaseKidney diseaseCell injuryMonocyte chemoattractant protein-1Alternative activation phenotypeChemoattractant protein-1Double knockout miceOrthologous mouse modelCell proliferative rateRenal functionMacrophage accumulationMacrophage infiltrationReceptor CCR2Cystic dilationMacrophage numbersFunctional improvementOxidative DNA damageMouse modelActivation phenotypeCyst expansion
2013
Chitinase 3-like 1 Regulates Cellular and Tissue Responses via IL-13 Receptor α2
He CH, Lee CG, Dela Cruz CS, Lee CM, Zhou Y, Ahangari F, Ma B, Herzog EL, Rosenberg SA, Li Y, Nour AM, Parikh CR, Schmidt I, Modis Y, Cantley L, Elias JA. Chitinase 3-like 1 Regulates Cellular and Tissue Responses via IL-13 Receptor α2. Cell Reports 2013, 4: 830-841. PMID: 23972995, PMCID: PMC3988532, DOI: 10.1016/j.celrep.2013.07.032.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisChitinase-3-Like Protein 1GlycoproteinsHumansInflammasomesInterleukin-13Interleukin-13 Receptor alpha2 SubunitLung NeoplasmsMacrophagesMAP Kinase Signaling SystemMelanomaMiceMice, Inbred C57BLOxidative StressProtein BindingTransforming Growth Factor betaWnt Signaling PathwayConceptsProtein kinase B/AktWnt/β-catenin signalingΒ-catenin signalingCritical roleGene familyMultimeric complexesProtein kinaseMacrophage mitogenDisease toleranceCell deathAntibacterial responseReceptor α2Antipathogen responsesChitinase 3IL-13Rα2IL-13 receptor α2Inflammasome activationBacterial killingKinaseOxidant injuryReceptorsMelanoma metastasesCHI3L1SignalingAktChitinase-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 migrationMacrophagesDistinct Macrophage Phenotypes Contribute to Kidney Injury and Repair
Lee S, Huen S, Nishio H, Nishio S, Lee HK, Choi BS, Ruhrberg C, Cantley LG. Distinct Macrophage Phenotypes Contribute to Kidney Injury and Repair. Journal Of The American Society Of Nephrology 2011, 22: 317-326. PMID: 21289217, PMCID: PMC3029904, DOI: 10.1681/asn.2009060615.Peer-Reviewed Original ResearchConceptsTubular cell proliferationProinflammatory macrophagesM2 phenotypeKidney injuryKidney repairInterstitial inflammatory cell infiltrateIschemia/reperfusion injuryRenal tubular cell proliferationTubular cell necrosisInflammatory cell infiltrateMacrophage-depleted miceDepletion of macrophagesIschemia/reperfusionBone marrow-derived macrophagesCell proliferationRenal tubular cellsMarrow-derived macrophagesAppearance of macrophagesLater time pointsKidney reperfusionTubule injuryCell infiltrateReperfusion injuryKidney damageMacrophage depletion