2020
Kidney tissue hypoxia dictates T cell–mediated injury in murine lupus nephritis
Chen PM, Wilson PC, Shyer JA, Veselits M, Steach HR, Cui C, Moeckel G, Clark MR, Craft J. Kidney tissue hypoxia dictates T cell–mediated injury in murine lupus nephritis. Science Translational Medicine 2020, 12 PMID: 32269165, PMCID: PMC8055156, DOI: 10.1126/scitranslmed.aay1620.Peer-Reviewed Original ResearchConceptsHypoxia-inducible factor-1Lupus nephritisT cellsTissue hypoxiaT-cell-mediated injuryCell-mediated injuryHIF-1 blockadeKidney tissue hypoxiaSystemic lupus erythematosusHuman lupus nephritisMurine lupus nephritisRenal injuryAutoimmune injuryLupus erythematosusAutoimmune diseasesImmune cellsRenal tissueMurine modelTissue damageMore hypoxicNephritisInjuryLow oxygen tensionOxygen tensionFactor 1
2014
Chemokine receptor Cxcr4 contributes to kidney fibrosis via multiple effectors
Yuan A, Lee Y, Choi U, Moeckel G, Karihaloo A. Chemokine receptor Cxcr4 contributes to kidney fibrosis via multiple effectors. American Journal Of Physiology. Renal Physiology 2014, 308: f459-f472. PMID: 25537742, PMCID: PMC4346747, DOI: 10.1152/ajprenal.00146.2014.Peer-Reviewed Original ResearchConceptsUnilateral ureteral obstructionCXCR4 expressionKidney fibrosisChemokine receptorsFibrotic responseSmooth muscle actin levelsG protein-coupled chemokine receptorsGrowth factorChronic kidney inflammationProgressive tissue injuryChronic kidney diseaseHigh CXCR4 expressionTGF-β1 levelsEffector cell typesProgression of fibrosisScarring/fibrosisFinal common pathwayPlatelet-derived growth factorRenal injuryKidney inflammationObstructed kidneysBone morphogenetic protein-7Renal fibrosisUreteral obstructionKidney diseaseRenalase 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
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
2009
Deletion of the Met receptor in the collecting duct decreases renal repair following ureteral obstruction
Ma H, Saenko M, Opuko A, Togawa A, Soda K, Marlier A, Moeckel GW, Cantley LG, Ishibe S. Deletion of the Met receptor in the collecting duct decreases renal repair following ureteral obstruction. Kidney International 2009, 76: 868-876. PMID: 19675527, DOI: 10.1038/ki.2009.304.Peer-Reviewed Original ResearchConceptsUreteral obstructionFibrotic responseKnockout miceMet receptorAcute tubular necrosisPlasminogen activator inhibitor-1Unilateral ureteral obstructionTubular cell proliferationActivator inhibitor-1Conditional knockout miceHepatocyte growth factorKidney injuryRenal injuryTubular necrosisFunctional recoveryInterstitial fibrosisCre miceRenal repairNephron injuryControl littermatesObstructionGrowth factorMiceInhibitor-1Injury
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
2005
Expression of Mediators of Renal Injury in the Remnant Kidney of ROP Mice Is Attenuated by Cyclooxygenase-2 Inhibition
Cheng H, Zhang M, Moeckel GW, Zhao Y, Wang S, Qi Z, Breyer MD, Harris RC. Expression of Mediators of Renal Injury in the Remnant Kidney of ROP Mice Is Attenuated by Cyclooxygenase-2 Inhibition. Nephron 2005, 101: e75-e85. PMID: 15995341, DOI: 10.1159/000086645.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsConnective Tissue Growth FactorCyclooxygenase 2 InhibitorsFibronectinsGlomerulosclerosis, Focal SegmentalImmediate-Early ProteinsIntercellular Signaling Peptides and ProteinsKidneyKidney TubulesMiceMice, Inbred StrainsNephrectomyProteinuriaProto-Oncogene Proteins c-metPyrazolesSulfonamidesTissue DistributionConceptsCyclooxygenase-2 inhibitionROP miceSC58236 treatmentRenal injuryRemnant kidneyImmunoreactive COX-2Immunoreactive TGF-beta1Selective COX-2 inhibitorsSystemic blood pressureConnective tissue growth factorSubtotal renal ablationRenal tubulointerstitial injuryExpression of mediatorsCOX-2 inhibitorsTissue growth factorCollagen IV mRNATubulointerstitial injuryBlood pressureRenal ablationSignificant albuminuriaCOX-2Macrophage markersMouse modelTGF-beta1Remnant group
2002
Cyclooxygenase-2 inhibitor blocks expression of mediators of renal injury in a model of diabetes and hypertension1
Cheng HF, Wang CJ, Moeckel GW, Zhang MZ, Mckanna JA, Harris RC. Cyclooxygenase-2 inhibitor blocks expression of mediators of renal injury in a model of diabetes and hypertension1. Kidney International 2002, 62: 929-939. PMID: 12164875, DOI: 10.1046/j.1523-1755.2002.00520.x.Peer-Reviewed Original ResearchConceptsCOX-2 expressionCOX-2 inhibitorsDiabetic groupRenal injuryDiabetic ratsImmunoreactive COX-2 expressionCortical thick ascending limbSelective COX-2 inhibitorsSystolic blood pressureModel of diabetesVascular endothelial growth factorDevelopment of glomerulosclerosisCOX-2 inhibitionThick ascending limbEndothelial growth factorMesangial sclerosis indexTubulointerstitial injuryDiabetic nephropathyBlood pressureChronic treatmentSubtotal nephrectomySclerosis indexBlood glucoseMacula densaRenal cortex