2022
Arginase-1 Is Required for Macrophage-Mediated Renal Tubule Regeneration
Shin NS, Marlier A, Xu L, Doilicho N, Linberg D, Guo J, Cantley LG. Arginase-1 Is Required for Macrophage-Mediated Renal Tubule Regeneration. Journal Of The American Society Of Nephrology 2022, 33: 1077-1086. PMID: 35577558, PMCID: PMC9161787, DOI: 10.1681/asn.2021121548.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsArginaseGranulocyte-Macrophage Colony-Stimulating FactorMacrophagesMiceMice, Inbred C57BLRegenerationReperfusion InjuryConceptsIschemia-reperfusion injuryTubular cell proliferationArginase-1Contralateral nephrectomyRenal repairFl/Littermate controlsTubular cellsReceptor 1GM-CSFRenal tubular cell proliferationRenal tubule regenerationMacrophage scavenger receptor 1Mannose receptor 1Cell proliferative responsesCell proliferationScavenger receptor 1Coculture of macrophagesDead cell debrisKidney injuryKidney repairRenal responseProinflammatory activationTubule regenerationMouse survivalKidney-Targeted Renalase Agonist Prevents Cisplatin-Induced Chronic Kidney Disease by Inhibiting Regulated Necrosis and Inflammation
Guo X, Xu L, Velazquez H, Chen TM, Williams RM, Heller DA, Burtness B, Safirstein R, Desir GV. Kidney-Targeted Renalase Agonist Prevents Cisplatin-Induced Chronic Kidney Disease by Inhibiting Regulated Necrosis and Inflammation. Journal Of The American Society Of Nephrology 2022, 33: 342-356. PMID: 34921111, PMCID: PMC8819981, DOI: 10.1681/asn.2021040439.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsAntineoplastic AgentsCell LineCisplatinCreatinineDisease Models, AnimalGene ExpressionGlomerular Filtration RateHepatitis A Virus Cellular Receptor 1HumansKidneyMiceMice, Inbred C57BLMice, KnockoutMonoamine OxidaseNanocapsulesPeptidesRenal Insufficiency, ChronicConceptsRenal proximal tubulesSingle-cell RNA sequencing analysisMesoscale nanoparticlesFirst doseCisplatin chemotherapyProximal tubulesAgonist peptideInduced Chronic Kidney DiseaseGenetic deletionNeck squamous cell carcinomaRNA sequencing analysisCisplatin-induced AKIKidney-targeted deliveryChronic kidney diseaseDevelopment of CKDSquamous cell carcinomaAdministration of cisplatinPlasma renalaseAdvanced headCell carcinomaInflammatory cytokinesKidney diseasePlasma creatinineSystemic administrationRegulated necrosis
2014
Cholesterol Sulfate and Cholesterol Sulfotransferase Inhibit Gluconeogenesis by Targeting Hepatocyte Nuclear Factor 4α
Shi X, Cheng Q, Xu L, Yan J, Jiang M, He J, Xu M, Stefanovic-Racic M, Sipula I, O'Doherty RM, Ren S, Xie W. Cholesterol Sulfate and Cholesterol Sulfotransferase Inhibit Gluconeogenesis by Targeting Hepatocyte Nuclear Factor 4α. Molecular And Cellular Biology 2014, 34: 485-497. PMID: 24277929, PMCID: PMC3911511, DOI: 10.1128/mcb.01094-13.Peer-Reviewed Original ResearchMeSH KeywordsAcetylationAnimalsBlotting, WesternCarcinoma, HepatocellularCell Line, TumorCell NucleusCells, CulturedCholesterol EstersCoenzyme A LigasesColforsinDiet, High-FatGene ExpressionGluconeogenesisGlucoseHepatocyte Nuclear Factor 4HumansInsulin ResistanceMiceMice, Inbred C57BLMice, ObeseMice, TransgenicObesityReverse Transcriptase Polymerase Chain ReactionSulfotransferasesConceptsDiet-induced obesityHepatocyte nuclear factor 4αNuclear factor 4αCholesterol sulfateLeptin-deficient miceTreatment of micePotential therapeutic targetPotential therapeutic agentExpression of SULT2B1bMetabolic abnormalitiesObese miceMetabolic disordersImportant metabolic regulatorGlucose metabolismTherapeutic targetTransgenic miceFed stateHepatic gluconeogenesisTherapeutic agentsMiceTransgenic overexpressionSULT2B1bMetabolic regulatorFunctional homeostasisInhibits gluconeogenesis
2012
5-Cholesten-3β,25-Diol 3-Sulfate Decreases Lipid Accumulation in Diet-Induced Nonalcoholic Fatty Liver Disease Mouse Model
Xu L, Kim JK, Bai Q, Zhang X, Kakiyama G, Min HK, Sanyal AJ, Pandak WM, Ren S. 5-Cholesten-3β,25-Diol 3-Sulfate Decreases Lipid Accumulation in Diet-Induced Nonalcoholic Fatty Liver Disease Mouse Model. Molecular Pharmacology 2012, 83: 648-658. PMID: 23258548, PMCID: PMC3583496, DOI: 10.1124/mol.112.081505.Peer-Reviewed Original ResearchMeSH KeywordsAcetyl-CoA CarboxylaseAcetyltransferasesAnimalsCholesterol EstersDiet, High-FatFas ReceptorFatty AcidsFatty LiverFemaleGene ExpressionGlucose Tolerance TestGlycerol-3-Phosphate O-AcyltransferaseHydroxycholesterolsInflammationInsulinInsulin ResistanceInterleukin-1alphaInterleukin-1betaLipid MetabolismLipidsLiverMiceMice, Inbred C57BLNon-alcoholic Fatty Liver DiseaseSignal TransductionSterol Regulatory Element Binding Protein 1Tumor Necrosis Factor-alphaConceptsNonalcoholic fatty liver diseaseHigh-fat dietLong-term treatmentAcute treatmentTolerance testLipid accumulationMouse modelDiet-induced NAFLD mouse modelNonalcoholic fatty liver disease (NAFLD) mouse modelSREBP-1cLipid homeostasisFatty liver diseaseLiver X receptor αNAFLD mouse modelGlucose tolerance testSerum lipid levelsInsulin tolerance testHepatic lipid accumulationDisease mouse modelDecreases lipid accumulationTumor necrosis factorLipid-induced inflammationAcetyl-CoA carboxylase 1X receptor αSREBP-1c expressionCholesterol metabolite, 5-cholesten-3β-25-diol-3-sulfate, promotes hepatic proliferation in mice
Zhang X, Bai Q, Kakiyama G, Xu L, Kim JK, Pandak WM, Ren S. Cholesterol metabolite, 5-cholesten-3β-25-diol-3-sulfate, promotes hepatic proliferation in mice. The Journal Of Steroid Biochemistry And Molecular Biology 2012, 132: 262-270. PMID: 22732306, PMCID: PMC3463675, DOI: 10.1016/j.jsbmb.2012.06.001.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCell CycleCell ProliferationCholesterolCholesterol EstersDNA ReplicationGene Expression RegulationHydrocarbons, FluorinatedHydroxycholesterolsLiverLiver X ReceptorsMiceMice, Inbred C57BLOrphan Nuclear ReceptorsSignal TransductionSulfonamidesSulfotransferasesTissue DistributionUp-RegulationConceptsLiver X receptorHepatic proliferationSynthetic LXR agonist T0901317LXR agonist T0901317PCNA labeling indexDose-dependent mannerSuppresses cell proliferationOxysterol sulfationOxysterol sulfotransferaseProliferation gene expressionAgonist T0901317Cholesterol metabolitesLabeling indexEndogenous ligandLiver proliferationX receptorHepatic DNA replicationHepatocyte proliferationSREBP-1cNovel regulatory pathwayPCR arrayCell proliferationAdministrationPotent regulatorOxysterols
2009
StAR Overexpression Decreases Serum and Tissue Lipids in Apolipoprotein E‐deficient Mice
Ning Y, Xu L, Ren S, Pandak WM, Chen S, Yin L. StAR Overexpression Decreases Serum and Tissue Lipids in Apolipoprotein E‐deficient Mice. Lipids 2009, 44: 511-519. PMID: 19373502, PMCID: PMC2911774, DOI: 10.1007/s11745-009-3299-1.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApolipoproteins EDisease Models, AnimalGene ExpressionLipidsMiceMice, Inbred C57BLPhosphoproteinsRecombinant ProteinsConceptsDeficient miceApolipoprotein ESerum HDL cholesterolSerum total cholesterolTreatment of dyslipidemiaPossible therapeutic roleSudan IV stainingMonths of ageNeutral lipid stainingSteroidogenic acute regulatory proteinDecreases SerumHDL cholesterolTotal cholesterolTriglyceride levelsAcute regulatory proteinTherapeutic roleStAR protein expressionCholesterol metabolismAnimal modelsAortic wallTissue lipidsLipid accumulationMiceRecombinant cytomegalovirusesLipid homeostasis