2017
Loss of the podocyte glucocorticoid receptor exacerbates proteinuria after injury
Zhou H, Tian X, Tufro A, Moeckel G, Ishibe S, Goodwin J. Loss of the podocyte glucocorticoid receptor exacerbates proteinuria after injury. Scientific Reports 2017, 7: 9833. PMID: 28852159, PMCID: PMC5575043, DOI: 10.1038/s41598-017-10490-z.Peer-Reviewed Original ResearchConceptsKnockout miceGlucocorticoid receptorNephrotic syndromeSimilar renal functionMainstay of therapyReceptor knockout miceTreatment of proteinuriaFoot process effacementMechanism of actionImmunomodulatory therapyRenal functionGlomerular injuryProtein excretionKO miceCommon disorderNephrotoxic serumPodocyte injuryPodocyte-specific deletionMouse modelSlit diaphragm proteinsWild-type podocytesProcess effacementProteinuriaUnstimulated conditionsKnockout animalsRenal recovery following orthotopic liver transplant after prolonged kidney injury: Perspectives on diagnosing hepatorenal syndrome and determining which patients should undergo simultaneous liver kidney transplantation
Card M, Moeckel G, Turner J. Renal recovery following orthotopic liver transplant after prolonged kidney injury: Perspectives on diagnosing hepatorenal syndrome and determining which patients should undergo simultaneous liver kidney transplantation. Journal Of Renal And Hepatic Disorders 2017, 1: 25-28. DOI: 10.15586/jrenhep.2017.20.Peer-Reviewed Original ResearchOrthotopic liver transplantHepatorenal syndromeRenal recoveryLiver transplantSimultaneous liver-kidney transplantSimultaneous liver-kidney transplantationLiver-kidney transplantSignificant renal recoveryLiver-kidney transplantationMonths of dialysisImmunoglobulin A (IgA) nephropathyCurrent diagnostic criteriaKidney injuryKidney transplantationRenal failureA NephropathyIgA depositsCase seriesGlomerular injuryGlomerular lesionsDiagnostic criteriaPatientsDiagnostic approachTransplantCirrhosis
2014
Podocyte-associated talin1 is critical for glomerular filtration barrier maintenance
Tian X, Kim JJ, Monkley SM, Gotoh N, Nandez R, Soda K, Inoue K, Balkin DM, Hassan H, Son SH, Lee Y, Moeckel G, Calderwood DA, Holzman LB, Critchley DR, Zent R, Reiser J, Ishibe S. Podocyte-associated talin1 is critical for glomerular filtration barrier maintenance. Journal Of Clinical Investigation 2014, 124: 1098-1113. PMID: 24531545, PMCID: PMC3934159, DOI: 10.1172/jci69778.Peer-Reviewed Original ResearchConceptsNephrotic syndromeFoot process effacementLoss of talin1Glomerular filtration barrierGlomerular injuryMurine modelProcess effacementKidney's glomerular filtration barrierFiltration barrierGlomerular basement membraneSevere proteinuriaKidney failurePharmacologic inhibitionSyndromeBarrier maintenanceCalpain activityIntegrin activationEpithelial cellsPodocytesModest reductionΒ1 integrin activationBasement membranePathogenesisInjuryCytoskeletal protein talin1
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
Nephrotoxicity From Chemotherapeutic Agents: Clinical Manifestations, Pathobiology, and Prevention/Therapy
Perazella MA, Moeckel GW. Nephrotoxicity From Chemotherapeutic Agents: Clinical Manifestations, Pathobiology, and Prevention/Therapy. Seminars In Nephrology 2010, 30: 570-581. PMID: 21146122, DOI: 10.1016/j.semnephrol.2010.09.005.Peer-Reviewed Original ResearchConceptsKidney lesionsChemotherapeutic agentsKidney injuryNephrotoxic chemotherapeutic agentsAcute kidney injuryChronic kidney injuryHost risk factorsDrug-induced nephrotoxicityPrevention/therapyGlomerular injuryClinical manifestationsRisk factorsRenal handlingNephrotoxicityVexing complicationInjuryLesionsDrugsInnate toxicityAgentsMost casesProteinuriaMedicationsComplicationsDysfunction
2009
Distinct Roles for Basal and Induced COX-2 in Podocyte Injury
Cheng H, Fan X, Guan Y, Moeckel GW, Zent R, Harris RC. Distinct Roles for Basal and Induced COX-2 in Podocyte Injury. Journal Of The American Society Of Nephrology 2009, 20: 1953-1962. PMID: 19643929, PMCID: PMC2736764, DOI: 10.1681/asn.2009010039.Peer-Reviewed Original ResearchMeSH KeywordsAlbuminuriaAnimalsAntibiotics, AntineoplasticApoptosisCell AdhesionCell Line, TransformedCell SurvivalCyclooxygenase 2DinoprostoneDoxorubicinGlomerulonephritisMaleMiceMice, Inbred StrainsMice, TransgenicPodocytesPuromycinReceptors, Prostaglandin EReceptors, ThromboxaneRNA, MessengerThromboxanesConceptsCyclooxygenase-2Thromboxane receptorCOX-2 knockout miceSelective deletionCOX-2 deletionInduced COX-2Receptor subtype 4COX-2 metabolitesFoot process effacementGlomerular injuryPodocyte injuryProstanoid receptorsAttenuated albuminuriaWild-type podocytesSubtype 4Transgenic miceProcess effacementTP antagonistPodocyte survivalInjuryMore prostaglandinsGenetic deletionMicePodocytesGreater expression
2007
Puromycin Induces Reversible Proteinuric Injury in Transgenic Mice Expressing Cyclooxygenase-2 in Podocytes
Jo YI, Cheng H, Wang S, Moeckel GW, Harris RC. Puromycin Induces Reversible Proteinuric Injury in Transgenic Mice Expressing Cyclooxygenase-2 in Podocytes. Nephron 2007, 107: e87-e94. PMID: 17890881, DOI: 10.1159/000108653.Peer-Reviewed Original ResearchConceptsCOX-2 expressionCOX-2-specific inhibitorsCOX-2 mRNATransgenic miceFoot process effacementDay 3COX-2Process effacementEndogenous COX-2 mRNAImmunoreactive COX-2Progressive renal diseaseCOX-2 overexpressionFoot process fusionCyclooxygenase-2 inhibitorRenal diseaseGlomerular injurySignificant albuminuriaCyclooxygenase-2Further injuryReal-time PCRDay 1Nephrin mRNADay 10AlbuminuriaMice
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