2018
Semaphorin 7A in circulating regulatory T cells is increased in autosomal-dominant polycystic kidney disease and decreases with tolvaptan treatment
Lee Y, Blount KL, Dai F, Thompson S, Scher JK, Bitterman S, Droher M, Herzog EL, Moeckel G, Karihaloo A, Dahl NK. Semaphorin 7A in circulating regulatory T cells is increased in autosomal-dominant polycystic kidney disease and decreases with tolvaptan treatment. Clinical And Experimental Nephrology 2018, 22: 906-916. PMID: 29453607, DOI: 10.1007/s10157-018-1542-x.Peer-Reviewed Original ResearchConceptsPeripheral blood mononuclear cellsAutosomal dominant polycystic kidney diseaseEnd-stage renal diseaseRenal fibrosisSEMA7A expressionADPKD patientsTolvaptan treatmentPolycystic kidney diseaseKidney diseaseNumber of PBMCsExpression of SEMA7ASubsequent renal fibrosisMarkers of inflammationRegulatory T cellsADPKD kidneysBlood mononuclear cellsImmunomodulating proteinsRenal diseaseMononuclear cellsSmall kidneysKidney fibrosisLiver fibrosisRenal cystsSemaphorin 7AT cells
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