2016
Isoforms of Spectrin and Ankyrin Reflect the Functional Topography of the Mouse Kidney
Stankewich MC, Moeckel GW, Ji L, Ardito T, Morrow JS. Isoforms of Spectrin and Ankyrin Reflect the Functional Topography of the Mouse Kidney. PLOS ONE 2016, 11: e0142687. PMID: 26727517, PMCID: PMC4703142, DOI: 10.1371/journal.pone.0142687.Peer-Reviewed Original ResearchConceptsBowman's capsuleEndothelial cellsFunctional topographyThick ascending loopGlomerular endothelial cellsProximal tubule cellsCapillary endothelial cellsAscending loopDistal tubulesDistal nephronTubule cellsTubular segmentsKidneyRodent kidneyWestern blottingMouse kidneyImmuno-electron microscopyThick loopAnkyrin GMetabolite traffickingSpectrin scaffoldHenleNephronCapsulePodocytes
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 inhibitionMacrophagesLoss of Polycystin-1 Inhibits Bicc1 Expression during Mouse Development
Lian P, Li A, Li Y, Liu H, Liang D, Hu B, Lin D, Jiang T, Moeckel G, Qin D, Wu G. Loss of Polycystin-1 Inhibits Bicc1 Expression during Mouse Development. PLOS ONE 2014, 9: e88816. PMID: 24594709, PMCID: PMC3940423, DOI: 10.1371/journal.pone.0088816.Peer-Reviewed Original ResearchConceptsAutosomal dominant polycystic kidney diseasePolycystic kidney diseasePolycystin-1Gene productsKidney developmentKidney diseaseRNA-binding proteinMouse kidney developmentPKD1 gene productEmbryonic day 8.5Human autosomal dominant polycystic kidney diseaseNew molecular linkTemporal expression patternsEarly ureteric budDominant polycystic kidney diseaseC. elegansHuman polycystic kidney diseaseMouse embryogenesisMouse developmentPostnatal kidney developmentMouse homologueCystic phenotypeExpression patternsMolecular linkMultiple species
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 changes