2015
Three-Dimensional Morphology by Multiphoton Microscopy with Clearing in a Model of Cisplatin-Induced CKD
Torres R, Velazquez H, Chang JJ, Levene MJ, Moeckel G, Desir GV, Safirstein R. Three-Dimensional Morphology by Multiphoton Microscopy with Clearing in a Model of Cisplatin-Induced CKD. Journal Of The American Society Of Nephrology 2015, 27: 1102-1112. PMID: 26303068, PMCID: PMC4814184, DOI: 10.1681/asn.2015010079.Peer-Reviewed Original ResearchConceptsAtubular glomeruliGlomerular capsuleRole of fibrosisModel of cisplatinNew mouse modelUseful morphologic informationMultiphoton microscopyTraditional histologic methodsRenal diseaseCisplatin therapyGlomerular volumePathologic changesRenal sectionsCKDMouse modelCisplatin effectCisplatin exposureImportant causeMild increaseCuboidal cellsHistologic methodsMorphologic informationFibrosisTherapyGlomeruli
2013
Aldosterone stimulates fibronectin synthesis in renal fibroblasts through mineralocorticoid receptor-dependent and independent mechanisms
Chen D, Chen Z, Park C, Centrella M, McCarthy T, Chen L, Al-Omari A, Moeckel GW. Aldosterone stimulates fibronectin synthesis in renal fibroblasts through mineralocorticoid receptor-dependent and independent mechanisms. Gene 2013, 531: 23-30. PMID: 23994292, DOI: 10.1016/j.gene.2013.08.047.Peer-Reviewed Original ResearchConceptsProgression of fibrosisFibronectin synthesisChronic kidney diseaseC-Jun NH2-terminal protein kinaseMineralocorticoid hormone aldosteroneKidney fibroblast cell lineTranscription factor c-JunExtracellular signal-regulated kinaseReceptor-dependent activationSignal-regulated kinaseDependent signaling pathwaysKidney injuryInterstitial fibrosisKidney diseaseMineralocorticoid receptorHormone aldosteroneAldosteroneRenal fibroblastsAnimal modelsProtein kinaseFibroblast cell lineFibronectin expressionKidneyFibrosisSubsequent phosphorylationMacrophage-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
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