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
2011
Podocyte vascular endothelial growth factor (Vegf164) overexpression causes severe nodular glomerulosclerosis in a mouse model of type 1 diabetes
Veron D, Bertuccio CA, Marlier A, Reidy K, Garcia AM, Jimenez J, Velazquez H, Kashgarian M, Moeckel GW, Tufro A. Podocyte vascular endothelial growth factor (Vegf164) overexpression causes severe nodular glomerulosclerosis in a mouse model of type 1 diabetes. Diabetologia 2011, 54: 1227-1241. PMID: 21318407, PMCID: PMC3397150, DOI: 10.1007/s00125-010-2034-z.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlotting, WesternChromatography, High Pressure LiquidCreatinineDiabetes Mellitus, Type 1Diabetic NephropathiesDisease Models, AnimalEnzyme-Linked Immunosorbent AssayImmunohistochemistryMiceMice, TransgenicMicroscopy, Electron, TransmissionPodocytesPolymerase Chain ReactionSemaphorin-3ATandem Mass SpectrometryVascular Endothelial Growth Factor AConceptsDiabetic nephropathyNodular glomerulosclerosisDiabetic glomerulopathyMouse modelMassive proteinuriaExcessive vascular endothelial growth factorTransgenic miceStreptozotocin-induced mouse modelVascular endothelial growth factor overexpressionGlomerular basement membrane thickeningAdvanced diabetic glomerulopathyControl diabetic miceOnset of diabetesBasement membrane thickeningVascular endothelial growth factorType 1 diabetesGrowth factor overexpressionAdult transgenic miceEndothelial growth factorVEGF receptor 2Kimmelstiel-WilsonSystemic VEGFDiabetic micePathogenic roleRenal morphology
2009
Urea promotes TonEBP expression and cellular adaptation in extreme hypertonicity
Kwon MS, Na KY, Moeckel G, Lee SD, Kwon HM. Urea promotes TonEBP expression and cellular adaptation in extreme hypertonicity. Pflügers Archiv - European Journal Of Physiology 2009, 459: 183. PMID: 19585141, DOI: 10.1007/s00424-009-0696-5.Peer-Reviewed Original ResearchConceptsCellular adaptationRegulation of TonEBPBody water homeostasisAmbient tonicityEpithelial cell lineCentral regulatorMDCK cellsTonEBPCellular proliferationWater homeostasisCell linesExpressionPrior adaptationInner medullaAdaptationRenal medullaAntidiuretic animalsHypertonicityRegulatorHomeostasisRegulationHigh levelsProliferationCellsModerate changesResolution of renal inflammation: a new role for NF-κB1 (p50) in inflammatory kidney diseases
Panzer U, Steinmetz OM, Turner JE, Meyer-Schwesinger C, von Ruffer C, Meyer TN, Zahner G, Gómez-Guerrero C, Schmid RM, Helmchen U, Moeckel GW, Wolf G, Stahl RA, Thaiss F. Resolution of renal inflammation: a new role for NF-κB1 (p50) in inflammatory kidney diseases. American Journal Of Physiology. Renal Physiology 2009, 297: f429-f439. PMID: 19458123, DOI: 10.1152/ajprenal.90435.2008.Peer-Reviewed Original ResearchMeSH KeywordsActive Transport, Cell NucleusAcute DiseaseAnimalsAntilymphocyte SerumBlotting, SouthwesternCells, CulturedChemokinesDisease Models, AnimalEndothelial CellsGlomerulonephritisImmunohistochemistryKidney GlomerulusLipopolysaccharidesMaleMiceMice, Inbred C57BLMice, KnockoutNephritisNF-kappa B p50 SubunitNF-kappa B p52 SubunitProtein MultimerizationRatsRats, WistarRemission, SpontaneousTime FactorsTranscription Factor RelATranscription Factor RelBConceptsNF-kappaBRenal inflammationTissue injuryNF-kappaB p50 knockout miceRenal inflammatory cell infiltrationHighest chemokine expressionP50 knockout miceRenal tissue injuryResolution of LPSGlomerular immune injuryInflammatory kidney diseasesInflammatory cell infiltrationRenal inflammatory diseaseProinflammatory gene expressionModel of glomerulonephritisTranscription factor NF-kappaBResolution periodImmune injuryRenal diseaseChemokine expressionAcute nephritisKidney diseaseCell infiltrationInflammatory diseasesInflammatory process
2004
PKHD1 protein encoded by the gene for autosomal recessive polycystic kidney disease associates with basal bodies and primary cilia in renal epithelial cells
Zhang MZ, Mai W, Li C, Cho SY, Hao C, Moeckel G, Zhao R, Kim I, Wang J, Xiong H, Wang H, Sato Y, Wu Y, Nakanuma Y, Lilova M, Pei Y, Harris RC, Li S, Coffey RJ, Sun L, Wu D, Chen XZ, Breyer MD, Zhao ZJ, McKanna JA, Wu G. PKHD1 protein encoded by the gene for autosomal recessive polycystic kidney disease associates with basal bodies and primary cilia in renal epithelial cells. Proceedings Of The National Academy Of Sciences Of The United States Of America 2004, 101: 2311-2316. PMID: 14983006, PMCID: PMC356947, DOI: 10.1073/pnas.0400073101.Peer-Reviewed Original ResearchConceptsAutosomal recessive polycystic kidney diseasePolycystic kidney diseaseKidney diseaseEpithelial cellsRecessive polycystic kidney diseaseHuman autosomal recessive polycystic kidney diseaseCultured renal cellsHepatic disease 1 (PKHD1) genePulmonary bronchiPCK rat kidneysRat modelDisease associatesPCK ratsPolycystic kidneysRenal epithelial cellsType 2Pathogenic basisRenal cellsRat kidneyPrimary ciliaHepatic cellsPolyclonal AbKidneyGene productsRats