2024
VCAM-1 mediates proximal tubule-immune cell cross talk in failed tubule recovery during AKI-to-CKD transition
Melchinger I, Guo K, Li X, Guo J, Cantley L, Xu L. VCAM-1 mediates proximal tubule-immune cell cross talk in failed tubule recovery during AKI-to-CKD transition. American Journal Of Physiology. Renal Physiology 2024, 327: f610-f622. PMID: 39116349, PMCID: PMC11483080, DOI: 10.1152/ajprenal.00076.2024.Peer-Reviewed Original ResearchAcute kidney injuryChronic kidney diseaseVCAM-1 expressionProximal tubule cellsVCAM-1Tubule cellsKidney Precision Medicine ProjectProinflammatory cytokinesAcute kidney injury to chronic kidney diseaseModel of chronic kidney diseaseExpression of vascular cell adhesion protein 1Cell adhesion pathwaysInflammatory response to injuryInjured proximal tubule cellsVascular cell adhesion protein 1Mouse model of chronic kidney diseaseRisk of progressionChronic kidney disease transitionIncreased immune cell adhesionVCAM-1-positive cellsOverexpression of VCAM-1Inhibition of NF-kB signalingActivation of NF-kBImmune cell adhesionSingle-cell transcriptome analysis
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