2019
Regulated necrosis and failed repair in cisplatin-induced chronic kidney disease
Landau SI, Guo X, Velazquez H, Torres R, Olson E, Garcia-Milian R, Moeckel GW, Desir GV, Safirstein R. Regulated necrosis and failed repair in cisplatin-induced chronic kidney disease. Kidney International 2019, 95: 797-814. PMID: 30904067, PMCID: PMC6543531, DOI: 10.1016/j.kint.2018.11.042.Peer-Reviewed Original ResearchConceptsChronic kidney diseaseKidney diseaseKidney injuryCisplatin-induced chronic kidney diseaseCisplatin-induced acute kidney injuryToll-like receptor 2Regulated necrosis pathwaysReversible kidney injuryAcute kidney injuryChronic kidney injuryProximal tubular damageKidney injury markersDoses of cisplatinEvidence of fibrosisMechanisms of progressionEffective chemotherapeutic agentWestern blot analysisFirst doseInjury markersIntraperitoneal cisplatinSignificant nephrotoxicityTubular damageKidney functionSecond doseCisplatin administration
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
2013
Macrophage-specific deletion of transforming growth factor-β1 does not prevent renal fibrosis after severe ischemia-reperfusion or obstructive injury
Huen SC, Moeckel GW, Cantley LG. Macrophage-specific deletion of transforming growth factor-β1 does not prevent renal fibrosis after severe ischemia-reperfusion or obstructive injury. American Journal Of Physiology. Renal Physiology 2013, 305: f477-f484. PMID: 23761668, PMCID: PMC3891258, DOI: 10.1152/ajprenal.00624.2012.Peer-Reviewed Original ResearchConceptsGrowth factor-β1Kidney injuryKidney diseaseRenal fibrosisTGF-β1Factor-β1Renal ischemia-reperfusion injuryChronic kidney diseaseIschemia-reperfusion injuryProgressive renal fibrosisMacrophage-specific deletionInnate immune responseMyeloid lineage cellsPersistence of macrophagesLater time pointsTubulointerstitial fibrosisFibrosis markersInterstitial fibrosisMacrophage infiltrationEffective therapyInjury modelObstructive injuryImmune responseTissue scarringFibrosis
2010
TGF-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 ResearchConceptsRenal 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
2005
Role of integrin α1β1 in the regulation of renal medullary osmolyte concentration
Moeckel GW, Zhang L, Chen X, Rossini M, Zent R, Pozzi A. Role of integrin α1β1 in the regulation of renal medullary osmolyte concentration. American Journal Of Physiology. Renal Physiology 2005, 290: f223-f231. PMID: 16106035, DOI: 10.1152/ajprenal.00371.2004.Peer-Reviewed Original ResearchConceptsIntegrin alpha1-null miceOsmolyte accumulationTonicity enhancer-binding proteinExtracellular matrix receptors integrinsOrganic osmolytesProtective organic osmolytesMEK inhibitor PD 98059Inositol uptakeInhibitor PD 98059Enhancer-binding proteinRenal medullary cellsTubular necrosisGene transcriptionOsmolyte transportersReceptor integrinPD 98059Altered signalingDifferent osmotic conditionsOsmolyte concentrationMammalian kidneyCell behaviorImportant mediatorERK1/2 phosphorylationOsmotic conditionsDuct cells