2022
Immune-mediated tubule atrophy promotes acute kidney injury to chronic kidney disease transition
Xu L, Guo J, Moledina DG, Cantley LG. Immune-mediated tubule atrophy promotes acute kidney injury to chronic kidney disease transition. Nature Communications 2022, 13: 4892. PMID: 35986026, PMCID: PMC9391331, DOI: 10.1038/s41467-022-32634-0.Peer-Reviewed Original ResearchMeSH KeywordsAcute Kidney InjuryAnimalsAtrophyKidneyKidney TubulesMiceRenal Insufficiency, ChronicReperfusion InjuryConceptsAcute kidney injuryKidney injuryT cellsChronic kidney disease transitionIschemia-reperfusion kidney injuryKidney disease transitionChronic kidney diseaseDepletion of neutrophilsGlomerular filtration rateT cell recruitmentTubular cell lossMacrophage persistenceProinflammatory neutrophilsTubule damageKidney atrophyContralateral kidneyNeutrophil numbersContralateral nephrectomyKidney diseaseTubule atrophyFiltration rateCell recruitmentMore macrophagesDay 14Day 5Characterization of temporospatial distribution of renal tubular casts by nephron tracking after ischemia-reperfusion injury
Shin NS, Marlier A, Xu L, Lam T, Cantley LG, Guo JK. Characterization of temporospatial distribution of renal tubular casts by nephron tracking after ischemia-reperfusion injury. American Journal Of Physiology. Renal Physiology 2022, 322: f322-f334. PMID: 35100823, PMCID: PMC8897010, DOI: 10.1152/ajprenal.00284.2021.Peer-Reviewed Original ResearchConceptsIschemia-reperfusion injuryCast formationGlomerular filtration rateTubular cast formationUrine 24 hDetached epithelial cellsDead cell debrisRenal recoveryRenal functionFiltration rateS3 tubulesTubular castsTubular cellsTubular nucleiKidney sectionsOuter medullaTrypsin levelsEntire nephronRenal tubular castsFuture interventionsInjurySelective lossTubule segmentsEpithelial cellsKidney
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
2011
Distinct 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
2001
HGF promotes adhesion of ATP-depleted renal tubular epithelial cells in a MAPK-dependent manner
Liu Z, Nickel C, Cantley L. HGF promotes adhesion of ATP-depleted renal tubular epithelial cells in a MAPK-dependent manner. American Journal Of Physiology. Renal Physiology 2001, 281: f62-f70. PMID: 11399647, DOI: 10.1152/ajprenal.2001.281.1.f62.Peer-Reviewed Original ResearchConceptsMitogen-activated protein kinaseATP-depleted cellsHepatocyte growth factorCell adhesionAddition of HGFATP depletionExtracellular signal-regulated kinase (ERK) phosphorylationMAPK-dependent mannerSignal-regulated kinase phosphorylationLoss of adhesionDuct 3 cellsEffects of HGFProtein kinaseERK activationMAPK pathwayKinase phosphorylationRenal tubular epithelial cellsEpithelial cellsAdherent cellsGrowth factorCellsATPTubular epithelial cellsPathwayAdhesionCell Surface Glypicans Are Low-Affinity Endostatin Receptors
Karumanchi S, Jha V, Ramchandran R, Karihaloo A, Tsiokas L, Chan B, Dhanabal M, Hanai J, Venkataraman G, Shriver Z, Keiser N, Kalluri R, Zeng H, Mukhopadhyay D, Chen R, Lander A, Hagihara K, Yamaguchi Y, Sasisekharan R, Cantley L, Sukhatme V. Cell Surface Glypicans Are Low-Affinity Endostatin Receptors. Molecular Cell 2001, 7: 811-822. PMID: 11336704, DOI: 10.1016/s1097-2765(01)00225-8.Peer-Reviewed Original ResearchConceptsHeparan sulfate glycosaminoglycansPotent anti-angiogenic proteinCell surface proteoglycansBranching morphogenesisEndothelial cellsGenetic studiesGlypicansExpression cloningSurface proteoglycansAntisense experimentsCell surfaceAnti-angiogenic proteinEndothelial cell surfaceLow-affinity receptorsSulfate glycosaminoglycansEndostatin bindingCellsReceptorsMorphogenesisEndostatin activityCloningProteinEndostatinBindingProteoglycans
1996
An 11-Amino Acid Sequence from c-met Initiates Epithelial Chemotaxis via Phosphatidylinositol 3-Kinase and Phospholipase C (∗)
Derman M, Chen J, Spokes K, Songyang Z, Cantley L. An 11-Amino Acid Sequence from c-met Initiates Epithelial Chemotaxis via Phosphatidylinositol 3-Kinase and Phospholipase C (∗). Journal Of Biological Chemistry 1996, 271: 4251-4255. PMID: 8626770, DOI: 10.1074/jbc.271.8.4251.Peer-Reviewed Original Research3T3 CellsAmino Acid SequenceAnimalsCell LineChemotaxisCloning, MolecularEpitheliumHepatocyte Growth FactorKidney TubulesMiceMolecular Sequence DataPeptide FragmentsPhosphatidylinositol 3-KinasesPhosphotransferases (Alcohol Group Acceptor)Platelet-Derived Growth FactorPoint MutationProto-Oncogene ProteinsProto-Oncogene Proteins c-metReceptor Protein-Tyrosine KinasesReceptors, Platelet-Derived Growth FactorRecombinant ProteinsTransfectionType C Phospholipases
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