2019
PD-1H (VISTA)–mediated suppression of autoimmunity in systemic and cutaneous lupus erythematosus
Han X, Vesely MD, Yang W, Sanmamed MF, Badri T, Alawa J, López-Giráldez F, Gaule P, Lee SW, Zhang JP, Nie X, Nassar A, Boto A, Flies DB, Zheng L, Kim TK, Moeckel GW, McNiff JM, Chen L. PD-1H (VISTA)–mediated suppression of autoimmunity in systemic and cutaneous lupus erythematosus. Science Translational Medicine 2019, 11 PMID: 31826980, DOI: 10.1126/scitranslmed.aax1159.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsArthritisAutoantibodiesAutoimmunityDendritic CellsHumansInflammationInterferon Type ILupus Erythematosus, CutaneousLupus Erythematosus, SystemicMembrane ProteinsMice, Inbred BALB CMice, Inbred MRL lprMyeloid CellsNeutrophilsReceptors, Antigen, T-CellSignal TransductionTerpenesUp-RegulationConceptsPlasmacytoid dendritic cellsDiscoid lupus erythematosusSystemic lupus erythematosusCutaneous lupus lesionsPD-1HLupus erythematosusLupus lesionsAutoimmune diseasesKO miceT cellsMyeloid cellsHuman systemic lupus erythematosusBALB/c backgroundCutaneous lupus erythematosusInappropriate immune responseProgression of lupusSystemic autoimmune diseaseImmune cell expansionSuppression of autoimmunityAgonistic monoclonal antibodyDeath-1 homologCutaneous lupusProinflammatory neutrophilsDendritic cellsDLE lesions
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