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 disease
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 injuryTGF-β Receptor Deletion in the Renal Collecting System Exacerbates Fibrosis
Gewin L, Bulus N, Mernaugh G, Moeckel G, Harris RC, Moses HL, Pozzi A, Zent R. TGF-β Receptor Deletion in the Renal Collecting System Exacerbates Fibrosis. Journal Of The American Society Of Nephrology 2010, 21: 1334-1343. PMID: 20576806, PMCID: PMC2938601, DOI: 10.1681/asn.2010020147.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCells, CulturedFibrosisKidneyKidney Tubules, CollectingMiceReceptors, Transforming Growth Factor betaUreteral ObstructionConceptsRenal collecting systemTGF-beta signalingRenal fibrosisReceptor deletionCollecting systemTGF-beta type II receptorUnilateral ureteral obstructionReceptor-mediated functionsRenal interstitial fibroblastsTGF-beta activationType II receptorParadoxic increaseUreteral obstructionII receptorsInterstitial fibroblastsInterstitial cellsFibrosisDuct cellsCollagen synthesisUreteric bud developmentInjuryMiceMatrix productionEnhanced levelsSignaling
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