2015
Human Polycystin-2 Transgene Dose-Dependently Rescues ADPKD Phenotypes in Pkd2 Mutant Mice
Li A, Tian X, Zhang X, Huang S, Ma Y, Wu D, Moeckel G, Somlo S, Wu G. Human Polycystin-2 Transgene Dose-Dependently Rescues ADPKD Phenotypes in Pkd2 Mutant Mice. American Journal Of Pathology 2015, 185: 2843-2860. PMID: 26435415, PMCID: PMC4607765, DOI: 10.1016/j.ajpath.2015.06.014.Peer-Reviewed Original ResearchConceptsAutosomal dominant polycystic kidney diseaseMouse modelADPKD phenotypeSevere cystic phenotypeWild-type miceDose-dependent mannerPolycystic kidney diseaseForms of ADPKDKidney diseasePancreatic cystsEffective treatmentFunctional restorationMutant miceTransgene doseMiceCyst formationReduced proliferationEpithelial cellsCystic phenotypeKidneyLiverFurther ameliorationPC2 activityPhenotypeMolecular genetic mechanisms
2014
Podocyte-Specific VEGF-A Gain of Function Induces Nodular Glomerulosclerosis in eNOS Null Mice
Veron D, Aggarwal PK, Velazquez H, Kashgarian M, Moeckel G, Tufro A. Podocyte-Specific VEGF-A Gain of Function Induces Nodular Glomerulosclerosis in eNOS Null Mice. Journal Of The American Society Of Nephrology 2014, 25: 1814-1824. PMID: 24578128, PMCID: PMC4116059, DOI: 10.1681/asn.2013070752.Peer-Reviewed Original ResearchConceptsNodular glomerulosclerosisGain of functionEndothelial nitric oxide synthase knockout miceNitric oxide synthase knockout miceGlomerular basement membrane thickeningENOS-null miceSynthase knockout miceBasement membrane thickeningWild-type miceCollagen IVArteriolar hyalinosisGlomerular nodulesGlomerular VEGFKimmelstiel-WilsonPronounced albuminuriaCreatinine clearanceRenal failureDiabetic nephropathyENOS deficiencyMassive proteinuriaDiabetic milieuMembrane thickeningPodocyte effacementDeposition of lamininKnockout miceRenalase Prevents AKI Independent of Amine Oxidase Activity
Wang L, Velazquez H, Moeckel G, Chang J, Ham A, Lee HT, Safirstein R, Desir GV. Renalase Prevents AKI Independent of Amine Oxidase Activity. Journal Of The American Society Of Nephrology 2014, 25: 1226-1235. PMID: 24511138, PMCID: PMC4033373, DOI: 10.1681/asn.2013060665.Peer-Reviewed Original ResearchConceptsIschemic injuryCatecholamine levelsRecombinant renalaseAmine oxidase activityHuman proximal tubular cellsCisplatin-induced AKITreatment of AKIWild-type miceHK-2 cellsProximal tubular cellsOxidase activityKidney injuryRenal injuryC-Jun N-terminal kinaseExtracellular signal-regulated kinaseP38 mitogen-activated protein kinaseToxic injuryRenalase proteinTubular cellsSignal-regulated kinaseIntracellular signaling cascadesRenalaseInjuryMitogen-activated protein kinaseN-terminal kinase
2013
NALP3-mediated inflammation is a principal cause of progressive renal failure in oxalate nephropathy
Knauf F, Asplin JR, Granja I, Schmidt IM, Moeckel GW, David RJ, Flavell RA, Aronson PS. NALP3-mediated inflammation is a principal cause of progressive renal failure in oxalate nephropathy. Kidney International 2013, 84: 895-901. PMID: 23739234, PMCID: PMC3772982, DOI: 10.1038/ki.2013.207.Peer-Reviewed Original ResearchConceptsProgressive renal failureRenal failureCalcium oxalate crystal depositionCrystal-associated diseasesOverproduction of oxalateWild-type miceHigh-oxalate dietNephropathy resultsOxalate nephropathyRenal histologyKidney diseaseOxalate dietInflammatory responseNALP3 expressionDietary oxalateIntestinal oxalateOxalate homeostasisSoluble oxalateNephropathyCrystal depositionMiceMultiple disordersNALP3DietInflammation
2011
Podocyte COX-2 Exacerbates Diabetic Nephropathy by Increasing Podocyte (Pro)renin Receptor Expression
Cheng H, Fan X, Moeckel GW, Harris RC. Podocyte COX-2 Exacerbates Diabetic Nephropathy by Increasing Podocyte (Pro)renin Receptor Expression. Journal Of The American Society Of Nephrology 2011, 22: 1240-1251. PMID: 21737546, PMCID: PMC3137572, DOI: 10.1681/asn.2010111149.Peer-Reviewed Original ResearchConceptsCOX-2 transgenic miceDiabetic nephropathyFoot process effacementCOX-2Transgenic miceGlomerular injuryReceptor expressionHigh glucoseRenin-angiotensin systemMesangial matrix expansionCOX-2 inhibitionWild-type miceCOX-2 inhibitorsCyclooxygenase-2 expressionGlomerular basement membraneStreptozotocin modelProgressive albuminuriaSegmental thickeningMesangial expansionDiabetic mellitusCell injuryAnimal modelsInjuryIncreased expressionNephropathy
2010
Identification and Regulation of Reticulon 4B (Nogo-B) in Renal Tubular Epithelial Cells
Marin EP, Moeckel G, Al-Lamki R, Bradley J, Yan Q, Wang T, Wright PL, Yu J, Sessa WC. Identification and Regulation of Reticulon 4B (Nogo-B) in Renal Tubular Epithelial Cells. American Journal Of Pathology 2010, 177: 2765-2773. PMID: 20971739, PMCID: PMC2993268, DOI: 10.2353/ajpath.2010.100199.Peer-Reviewed Original ResearchConceptsUnilateral ureteral obstructionAcute tubular necrosisEpithelial cellsRenal tubular epithelial cellsMurine kidneyIschemia/reperfusionMeasurement of fibrosisDistal nephron segmentsRecruitment of macrophagesWild-type miceInflammatory gene expressionTubular epithelial cellsDe novo expressionHuman biopsy specimensRenal injuryTubular necrosisUreteral obstructionWT miceVascular injuryHistological damageBiopsy specimensCortical tubulesDeficient miceMacrophage recruitmentTissue injury
2008
NFATc1 Identifies a Population of Proximal Tubule Cell Progenitors
Langworthy M, Zhou B, de Caestecker M, Moeckel G, Baldwin HS. NFATc1 Identifies a Population of Proximal Tubule Cell Progenitors. Journal Of The American Society Of Nephrology 2008, 20: 311-321. PMID: 19118153, PMCID: PMC2637056, DOI: 10.1681/asn.2008010094.Peer-Reviewed Original ResearchConceptsProximal tubular cell injuryBALB/c miceAcute kidney injuryTubular cell injuryWild-type miceProximal tubule segmentsKidney injurySerum creatinineCalcineurin inhibitorsC miceSustained injuryNFATc1 activityPTC proliferationCell injuryProximal tubulesNFATc1 expressionSevere injuriesTubule cellsInjuryMercuric chlorideEpithelial regenerationNephron segmentsCyclosporin AMiceTubule segments
2007
Overexpression of Cyclooxygenase-2 Predisposes to Podocyte Injury
Cheng H, Wang S, Jo YI, Hao CM, Zhang M, Fan X, Kennedy C, Breyer MD, Moeckel GW, Harris RC. Overexpression of Cyclooxygenase-2 Predisposes to Podocyte Injury. Journal Of The American Society Of Nephrology 2007, 18: 551-559. PMID: 17202413, DOI: 10.1681/asn.2006090990.Peer-Reviewed Original ResearchConceptsCOX-2 expressionBALB/c miceFoot process effacementTransgenic miceC micePodocyte injuryProcess effacementCOX-2 transgenic miceImmunoreactive COX-2 expressionCOX-2 mRNA expressionNephrin promoterLong-term treatmentCOX-2 overexpressionTransgenic mouse kidneyCyclooxygenase-2 expressionWild-type miceWild-type littermatesCOX-2 mRNARenal injuryRenal ablationAdriamycin nephropathyMore albuminuriaAdriamycin administrationFurther injuryCOX-2
2006
Glomerular injury is exacerbated in diabetic integrin α1-null mice
Zent R, Yan X, Su Y, Hudson B, Borza D, Moeckel G, Qi Z, Sado Y, Breyer M, Voziyan P, Pozzi A. Glomerular injury is exacerbated in diabetic integrin α1-null mice. Kidney International 2006, 70: 460-470. PMID: 16775606, DOI: 10.1038/sj.ki.5000359.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBasement MembraneCell DivisionCell MovementCells, CulturedCollagen Type IVDiabetes Mellitus, ExperimentalDiabetic NephropathiesDisease Models, AnimalGlomerular Filtration RateGlucoseGlycation End Products, AdvancedIntegrin alpha1Integrin alpha1beta1MaleMesangial CellsMiceMice, Inbred BALB CMice, KnockoutOxidative StressReactive Oxygen SpeciesConceptsGlomerular filtration rateWild-type miceDiabetic wild-type miceDiabetic nephropathyGlomerular injuryCollagen depositionMesangial cellsGlomerular basement membrane thickeningCollagen IVGlomerular collagen IVIntegrin alpha1-null miceNon-diabetic miceIntegrin α1-null miceBasement membrane thickeningDiabetic mutant mouseGlomerular collagen depositionROS productionCollagen IV productionSTZ injectionWeek 24Renal diseaseGlomerular depositionWeek 36Week 12Filtration rate
2004
Lack of Integrin α1β1 Leads to Severe Glomerulosclerosis after Glomerular Injury
Chen X, Moeckel G, Morrow JD, Cosgrove D, Harris RC, Fogo AB, Zent R, Pozzi A. Lack of Integrin α1β1 Leads to Severe Glomerulosclerosis after Glomerular Injury. American Journal Of Pathology 2004, 165: 617-630. PMID: 15277235, PMCID: PMC1618576, DOI: 10.1016/s0002-9440(10)63326-3.Peer-Reviewed Original ResearchConceptsSevere glomerulosclerosisGlomerular injuryIntegrin alpha1-null miceSeverity of fibrosisCollagen IV accumulationWild-type miceHost genetic susceptibilityMetabolism of collagenReactive oxygen species productionFibrotic lesionsIntegrin alpha1beta1Oxygen species productionAdriamycin treatmentMesangial cellsMatrix accumulationGenetic susceptibilityInjuryGlomerulosclerosisFibrosisCell proliferationROS productionSpecies productionROS synthesisIntegrin α1β1Mice
2003
Importance of Functional EGF Receptors in Recovery from Acute Nephrotoxic Injury
Wang Z, Chen JK, Wang SW, Moeckel G, Harris RC. Importance of Functional EGF Receptors in Recovery from Acute Nephrotoxic Injury. Journal Of The American Society Of Nephrology 2003, 14: 3147-3154. PMID: 14638913, DOI: 10.1097/01.asn.0000098681.56240.1a.Peer-Reviewed Original ResearchConceptsAcute nephrotoxic injuryTubular injuryNephrotoxic injurySerum blood urea nitrogenEGF receptorDUTP nick end labeling stainingNick end labeling stainingRenal tubular injuryBlood urea nitrogenWild-type miceReceptor tyrosine kinase activityTubule injuryRenal compromiseCreatinine levelsRenal expressionAcute injuryHistologic evidenceExogenous administrationSuch injuriesLabeling stainingKidney's abilityUrea nitrogenRate of recoveryInjuryMice