2022
Regulation of glomerulotubular balance. IV. Implication of aquaporin 1 in flow-dependent proximal tubule transport and cell volume
Du Z, Yan Q, Shen E, Weinstein A, Wang T. Regulation of glomerulotubular balance. IV. Implication of aquaporin 1 in flow-dependent proximal tubule transport and cell volume. American Journal Of Physiology. Renal Physiology 2022, 323: f642-f653. PMID: 36108052, PMCID: PMC9705020, DOI: 10.1152/ajprenal.00167.2022.Peer-Reviewed Original ResearchConceptsWater channel aquaporin-1Proximal tubulesKO miceAquaporin-1Water reabsorptionMouse PTNo significant differenceWild-typeTight junctionsRat kidneyAquaporin-1 knockoutSignificant differenceAcid-base parametersKidney proximal tubulesRenal clearance experimentsWT miceKnockout miceUrine flowFlow stimulationFluid absorptionUrine pHClearance experimentsMouse kidneyMiceRats
2021
Restoration of proximal tubule flow-activated transport prevents cyst growth in polycystic kidney disease
Du Z, Tian X, Ma M, Somlo S, Weinstein AM, Wang T. Restoration of proximal tubule flow-activated transport prevents cyst growth in polycystic kidney disease. JCI Insight 2021, 6: e146041. PMID: 33886508, PMCID: PMC8262298, DOI: 10.1172/jci.insight.146041.Peer-Reviewed Original ResearchConceptsGlomerular filtration rateGlomerulotubular balanceRenal cyst formationCyst formationReceptor 1 antagonistPolycystic kidney diseaseKidney weightUntreated miceDA1 antagonistControl miceKidney diseaseFiltration rateFractional reabsorptionCystic indexMouse modelCyst growthConditional KOHCO3- absorptionHeterozygous miceSame antagonistsMicePT transportAntagonistEpithelial ciliaHCO3- transportDeletion of Cdh16 Ksp-cadherin leads to a developmental delay in the ability to maximally concentrate urine in mouse
Thomson R, Dynia DW, Burlein S, Thomson BR, Booth C, Knauf F, Wang T, Aronson P. Deletion of Cdh16 Ksp-cadherin leads to a developmental delay in the ability to maximally concentrate urine in mouse. American Journal Of Physiology. Renal Physiology 2021, 320: f1106-f1122. PMID: 33938239, PMCID: PMC8285649, DOI: 10.1152/ajprenal.00556.2020.Peer-Reviewed Original ResearchConceptsKsp-cadherinCell adhesion moleculeAtypical memberKidney developmentMammalian kidneyAdult mammalian kidneyBasolateral membraneNormal kidney developmentEpithelial cellsAdhesion moleculesMutant animalsExpression analysisSpecific expressionE-cadherin expressionWestern blot analysisEpithelial phenotypePrincipal proteinE-cadherinBlot analysisMouse linesAquaporin-2CadherinCritical roleDevelopmental delayKnockout mice
2019
Sex difference in kidney electrolyte transport II: impact of K+ intake on thiazide-sensitive cation excretion in male and female mice
Li J, Xu S, Yang L, Yang J, Wang CJ, Weinstein AM, Palmer LG, Wang T. Sex difference in kidney electrolyte transport II: impact of K+ intake on thiazide-sensitive cation excretion in male and female mice. American Journal Of Physiology. Renal Physiology 2019, 317: f967-f977. PMID: 31390232, PMCID: PMC6843050, DOI: 10.1152/ajprenal.00125.2019.Peer-Reviewed Original ResearchConceptsHK dietCation excretionWT animalsFemale animalsMale animalsSex differencesRenal clearance experimentsGlomerular filtration rateR KO miceExchanger isoform 3Distal NaHK intakeWestern blot analysisFractional excretionUrine volumeFiltration rateFemale miceKO miceNHE3 abundanceClearance experimentsNCC abundanceLittle sex differenceKnockout miceENaC expressionExcretion
2018
Potassium conservation is impaired in mice with reduced renal expression of Kir4.1
Malik S, Lambert E, Zhang J, Wang T, Clark H, Cypress M, Goldman B, Porter GA, Pena S, Nino W, Gray D. Potassium conservation is impaired in mice with reduced renal expression of Kir4.1. American Journal Of Physiology. Renal Physiology 2018, 315: f1271-f1282. PMID: 30110571, PMCID: PMC6293297, DOI: 10.1152/ajprenal.00022.2018.Peer-Reviewed Original ResearchMeSH KeywordsAlkalosisAnimalsAquaporin 3Gene Knockdown TechniquesGenotypeHypercalcemiaHyperkalemiaHypernatremiaKidney Concentrating AbilityMice, Inbred C57BLMice, KnockoutNephronsPhenotypePhosphorylationPotassium Channels, Inwardly RectifyingPotassium, DietaryRenal ReabsorptionSolute Carrier Family 12, Member 3ConceptsMg-free dietSevere urinary concentrating defectReduced renal expressionRenal K wastingSeSAME/EAST syndromeDistal convoluted tubuleKir4.1 protein expressionWild-type miceUrinary concentrating defectCre-LoxP methodologyAquaporin 3 expressionRelative hypercalcemiaRenal expressionPotassium conservationMetabolic alkalosisNCC expressionChannel Kir4.1Distal nephronKnockout miceConvoluted tubulesCotransporter expressionEAST syndromeHypokalemiaMiceReduced expression
2017
Urinary bladder hypertrophy characteristic of male ROMK Bartter’s mice does not occur in female mice
Kim JM, Xu S, Guo X, Hu H, Dong K, Wang T. Urinary bladder hypertrophy characteristic of male ROMK Bartter’s mice does not occur in female mice. AJP Regulatory Integrative And Comparative Physiology 2017, 314: r334-r341. PMID: 29092859, PMCID: PMC5899254, DOI: 10.1152/ajpregu.00315.2017.Peer-Reviewed Original ResearchConceptsKO miceBladder hypertrophyBladder weightUrinary bladder hypertrophyRenal outer medullary potassium channelSeverity of hydronephrosisWild-type miceROMK knockout miceBladder capacityDetrusor muscleWT miceUrinary tractBartter's syndromeFemale miceSalt wastingHydronephrosisKnockout miceROMK expressionMiceBladderHypertrophyPotassium channelsMRNA levelsSignificant enlargementSyndromeGender difference in kidney electrolyte transport. I. Role of AT1a receptor in thiazide-sensitive Na+-Cl− cotransporter activity and expression in male and female mice
Li J, Hatano R, Xu S, Wan L, Yang L, Weinstein AM, Palmer L, Wang T. Gender difference in kidney electrolyte transport. I. Role of AT1a receptor in thiazide-sensitive Na+-Cl− cotransporter activity and expression in male and female mice. American Journal Of Physiology. Renal Physiology 2017, 313: f505-f513. PMID: 28566500, PMCID: PMC5582908, DOI: 10.1152/ajprenal.00087.2017.Peer-Reviewed Original ResearchMeSH KeywordsAngiotensin IIAnimalsDiuresisFemaleHydrochlorothiazideKidneyMaleMice, KnockoutNatriuresisPhenotypeProtein Serine-Threonine KinasesReceptor, Angiotensin, Type 1Receptors, DrugSex CharacteristicsSodium Chloride SymportersSodium-Hydrogen Exchanger 3Sodium-Hydrogen ExchangersSolute Carrier Family 12, Member 3ConceptsUrine volumeKO miceCotransporter activityRenal clearance experimentsReceptor knockout miceGlomerular filtration rateBolus intravenous injectionDelivery of NaClNCC protein expressionGender differencesFiltration rateFemale miceAT1A receptorClearance experimentsKO animalsIntravenous injectionNCC expressionDistal nephronFractional NaKnockout miceMale KOProximal tubulesHCTZMiceNHE3 expression
2016
Kidney Tubular Ablation of Ocrl/Inpp5b Phenocopies Lowe Syndrome Tubulopathy
Inoue K, Balkin DM, Liu L, Nandez R, Wu Y, Tian X, Wang T, Nussbaum R, De Camilli P, Ishibe S. Kidney Tubular Ablation of Ocrl/Inpp5b Phenocopies Lowe Syndrome Tubulopathy. Journal Of The American Society Of Nephrology 2016, 28: 1399-1407. PMID: 27895154, PMCID: PMC5407733, DOI: 10.1681/asn.2016080913.Peer-Reviewed Original ResearchConceptsEarly embryonic lethalityTransporter 5Dent's diseaseIndependent endocytosisEmbryonic lethalityRedundant functionsType 2 inositolHuman phenotypesProximal tubule endocytosisOculocerebrorenal syndromeGenetic ablationCellular levelGermline knockoutLowe syndromeEndocytosisMouse backgroundMice resultsMutationsInositolLow molecular weight proteinuriaINPP5BParalogsProximal tubule functionDramatic effectOCRL
2013
Proximal tubule specific knockout of the Na+/H+ exchanger NHE3: effects on bicarbonate absorption and ammonium excretion
Li H, Du Z, Barone S, Rubera I, McDonough A, Tauc M, Zahedi K, Wang T, Soleimani M. Proximal tubule specific knockout of the Na+/H+ exchanger NHE3: effects on bicarbonate absorption and ammonium excretion. Journal Of Molecular Medicine 2013, 91: 951-963. PMID: 23508938, PMCID: PMC3730089, DOI: 10.1007/s00109-013-1015-3.Peer-Reviewed Original ResearchConceptsNa+/H+ exchanger NHE3Proximal convoluted tubulesKO miceMetabolic acidosisBicarbonate reabsorptionDays of acid loadingIsolated proximal convoluted tubulesConvoluted tubulesIn vitro microperfusion studyCompared to WT miceNHE3 knockout miceProximal tubule NHE3Acid loadNH4Cl acid loadMild metabolic acidosisWT miceNHE3Microperfusion studiesKnockout miceBicarbonate absorptionMutant miceVolume reabsorptionFloxed miceNH4Cl loadingTransgenic miceOlfactory receptor responding to gut microbiota-derived signals plays a role in renin secretion and blood pressure regulation
Pluznick JL, Protzko RJ, Gevorgyan H, Peterlin Z, Sipos A, Han J, Brunet I, Wan LX, Rey F, Wang T, Firestein SJ, Yanagisawa M, Gordon JI, Eichmann A, Peti-Peterdi J, Caplan MJ. Olfactory receptor responding to gut microbiota-derived signals plays a role in renin secretion and blood pressure regulation. Proceedings Of The National Academy Of Sciences Of The United States Of America 2013, 110: 4410-4415. PMID: 23401498, PMCID: PMC3600440, DOI: 10.1073/pnas.1215927110.Peer-Reviewed Original ResearchConceptsShort-chain fatty acidsRenin secretionBlood pressureGut microbiotaG protein-coupled receptor 41Acute hypotensive responseRenal juxtaglomerular apparatusSmall resistance vesselsMicrobiota-derived signalsModulate blood pressureBlood pressure regulationWild-type miceSmooth muscle cellsG protein-coupled receptorsGPR41 expressionOlfactory receptorsHypotensive responseProtein-coupled receptorsSCFA receptorsResistance vesselsJuxtaglomerular apparatusAntibiotic treatmentOlfr78Receptor 41Knockout mice
2012
Regulation of glomerulotubular balance. II. Impact of angiotensin II on flow-dependent transport
Du Z, Wan L, Yan Q, Weinbaum S, Weinstein A, Wang T. Regulation of glomerulotubular balance. II. Impact of angiotensin II on flow-dependent transport. American Journal Of Physiology. Renal Physiology 2012, 303: f1507-f1516. PMID: 22952281, PMCID: PMC3532483, DOI: 10.1152/ajprenal.00277.2012.Peer-Reviewed Original ResearchMeSH KeywordsAngiotensin IIAngiotensin II Type 1 Receptor BlockersAnimalsBicarbonatesBiological TransportEnzyme InhibitorsFemaleHemostasisIn Vitro TechniquesKidney GlomerulusKidney TubulesLosartanMacrolidesMiceMice, KnockoutModels, AnimalProton-Translocating ATPasesReceptor, Angiotensin, Type 1SodiumSodium-Hydrogen Exchanger 3Sodium-Hydrogen ExchangersConceptsNa(+)-H(+) exchanger 3Mouse tubulesImpact of angiotensin IIH-ATPaseMicroperfused in vitroAT(2) receptorsAT(1A) receptorFlow-mediated changesH-ATPase activityParacellular Cl(-Receptor availabilityAngiotensin IIAT(1ARegulate Na(+Increased Na(+Local angiotensinBasolateral transportJ(HCO3Mouse kidneyNet fluidInhibitor bafilomycinProtein levelsMiceReceptorsTubulesGenetic modifiers of hypertension in soluble guanylate cyclase α1–deficient mice
Buys E, Raher M, Kirby A, Mohd S, Baron D, Hayton S, Tainsh L, Sips P, Rauwerdink K, Yan Q, Tainsh R, Shakartzi H, Stevens C, Decaluwé K, da Gloria Rodrigues-Machado M, Malhotra R, Van de Voorde J, Wang T, Brouckaert P, Daly M, Bloch K. Genetic modifiers of hypertension in soluble guanylate cyclase α1–deficient mice. Journal Of Clinical Investigation 2012, 122: 2316-2325. PMID: 22565307, PMCID: PMC3366402, DOI: 10.1172/jci60119.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCyclic GMPEndothelium, VascularFemaleGenetic LinkageGenome, HumanGuanylate CyclaseHumansHypertensionMaleMiceMice, KnockoutQuantitative Trait LociRatsReceptors, Cytoplasmic and NuclearReninRenin-Angiotensin SystemSecond Messenger SystemsSoluble Guanylyl CyclaseSpecies SpecificityVasodilationConceptsRenin-angiotensin-aldosterone systemRenin-angiotensin-aldosterone system inhibitionRelaxation of vascular smooth muscleVascular smooth muscleInducing relaxation of vascular smooth muscleNitric oxideEndothelium-dependent vasorelaxationSubunit of soluble guanylate cyclaseSoluble guanylate cyclaseImproving endothelium-dependent vasorelaxationSmooth muscleQuantitative trait lociArterial pressureMale miceMouse strainsNO/cGMP signalingInduced relaxationAssociated with increased activityHypertensionGuanylate cyclaseBlood flowMiceGenetic modifiersReceptor componentsGenetic factors
2011
Renal outer medullary potassium channel knockout models reveal thick ascending limb function and dysfunction
Wang T. Renal outer medullary potassium channel knockout models reveal thick ascending limb function and dysfunction. Clinical And Experimental Nephrology 2011, 16: 49-54. PMID: 22038261, DOI: 10.1007/s10157-011-0495-0.Peer-Reviewed Original ResearchConceptsThick ascending limbIon transporter expressionRenal outer medullary potassium channelBartter's syndromeInward rectifier potassium channelPotassium channelsSmall-conductance K channelsROMK null miceMedullary thick ascending limbType II Bartter's syndromeSimilar phenotypeMammalian kidneyApical membraneK channelsROMK knockout miceKnockout modelsChannel activityChannel mutationsRenal functionLimb functionNull micePhysiological conditionsSalt wastingTransporter expressionPathophysiological conditionsChloride Channel (Clc)-5 Is Necessary for Exocytic Trafficking of Na+/H+ Exchanger 3 (NHE3)*
Lin Z, Jin S, Duan X, Wang T, Martini S, Hulamm P, Cha B, Hubbard A, Donowitz M, Guggino SE. Chloride Channel (Clc)-5 Is Necessary for Exocytic Trafficking of Na+/H+ Exchanger 3 (NHE3)*. Journal Of Biological Chemistry 2011, 286: 22833-22845. PMID: 21561868, PMCID: PMC3123051, DOI: 10.1074/jbc.m111.224998.Peer-Reviewed Original ResearchConceptsKO miceTrafficking of NHE3Proximal tubulesOpossum kidney cellsNHE3 activityDent's diseaseClC-5Surface expressionNHE3 surface expressionKidney cellsRenal proximal tubulesTotal protein levelsChloride/proton exchangerRates of basalReduced surface expressionKnockdown cellsParathyroid hormoneWT miceDegree of inhibitionCLCN5 geneSurface NHE3MiceTubule perfusionReduced expressionTwo-photon microscopyDifferential regulation of ROMK (Kir1.1) in distal nephron segments by dietary potassium
Wade JB, Fang L, Coleman RA, Liu J, Grimm PR, Wang T, Welling PA. Differential regulation of ROMK (Kir1.1) in distal nephron segments by dietary potassium. American Journal Of Physiology. Renal Physiology 2011, 300: f1385-f1393. PMID: 21454252, PMCID: PMC3119145, DOI: 10.1152/ajprenal.00592.2010.Peer-Reviewed Original ResearchConceptsDistal nephronDistal nephron segmentsRenal K secretionROMK knockout miceDietary potassiumExtent of expressionKnockout miceK secretionROMK expressionNephron segmentsNew antibodiesApical labelingPhysiological stimuliNephronROMKAntibodiesROMK channelsApical expressionChannel localizationChannel functionDifferential regulationLarge increaseDCT2Different regulatory mechanismsExtensive pattern
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 injury
2009
Inward rectifier channel, ROMK, is localized to the apical tips of glial‐like cells in mouse taste buds
Dvoryanchikov G, Sinclair M, Perea‐Martinez I, Wang T, Chaudhari N. Inward rectifier channel, ROMK, is localized to the apical tips of glial‐like cells in mouse taste buds. The Journal Of Comparative Neurology 2009, 517: 1-14. PMID: 19708028, PMCID: PMC3104395, DOI: 10.1002/cne.22152.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsFluorescent Antibody TechniqueGap JunctionsGlutamate DecarboxylaseGreen Fluorescent ProteinsImmunohistochemistryKidneyMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicNeurogliaPhospholipase C betaPotassium Channels, Inwardly RectifyingProtein IsoformsReverse Transcriptase Polymerase Chain ReactionRNA, MessengerTaste BudsTight JunctionsConceptsTaste budsTaste cellsTight junctionsHyperpolarized resting membrane potentialInwardly rectifying K channelsMouse taste budsRT-PCRApical tight junctionsMouse taste cellsInward rectifier channelsFungiform taste budsReverse-transcription polymerase chain reactionGlial cell markersQuantitative (q)RT-PCRGlial-like cellsROMK mRNAApical tipExtracellular K(+Rectifier channelsCell markersPolymerase chain reactionK channelsTransgenic miceAction potentialsBudsFunctional expression of the olfactory signaling system in the kidney
Pluznick JL, Zou DJ, Zhang X, Yan Q, Rodriguez-Gil DJ, Eisner C, Wells E, Greer CA, Wang T, Firestein S, Schnermann J, Caplan MJ. Functional expression of the olfactory signaling system in the kidney. Proceedings Of The National Academy Of Sciences Of The United States Of America 2009, 106: 2059-2064. PMID: 19174512, PMCID: PMC2644163, DOI: 10.1073/pnas.0812859106.Peer-Reviewed Original ResearchConceptsGlomerular filtration ratePlasma renin levelsMacula densa cellsCOX-2 expressionRenal distal nephronOlfactory G-proteinMDS cell linesOlfactory receptorsRenin levelsRenin secretionFiltration rateNNOS activityTubuloglomerular feedbackDistal nephronOlfactory epitheliumRenal tubulesGFR regulationAdenylate cyclaseG proteinsCell linesSensory roleKidneyFunctional expressionOlfactionExpression
2008
Disruption of Myosin 1e Promotes Podocyte Injury
Krendel M, Kim SV, Willinger T, Wang T, Kashgarian M, Flavell RA, Mooseker MS. Disruption of Myosin 1e Promotes Podocyte Injury. Journal Of The American Society Of Nephrology 2008, 20: 86-94. PMID: 19005011, PMCID: PMC2615733, DOI: 10.1681/asn.2007111172.Peer-Reviewed Original ResearchConceptsChronic renal injuryNormal glomerular filtrationGlomerular basement membraneRenal injuryKidney inflammationPodocyte foot processesGlomerular diseasePodocyte injuryGlomerular filtrationRenal tissueFoot processesPodocyte functionBasement membraneInjuryUltrastructural levelDiseaseMiceType IProteinuriaInflammationKidneyImportant rolePodocytesFemale ROMK null mice manifest more severe Bartter II phenotype on renal function and higher PGE2 production
Yan Q, Yang X, Cantone A, Giebisch G, Hebert S, Wang T. Female ROMK null mice manifest more severe Bartter II phenotype on renal function and higher PGE2 production. AJP Regulatory Integrative And Comparative Physiology 2008, 295: r997-r1004. PMID: 18579648, PMCID: PMC2536865, DOI: 10.1152/ajpregu.00051.2007.Peer-Reviewed Original ResearchConceptsROMK null miceFemale null miceNull miceRenal functionSurvival rateExtent of hydronephrosisDegree of hydronephrosisSeverity of hydronephrosisHigher PGE2 productionHydronephrotic miceLower GFRSyndrome pathophysiologyNg/24 hAcid-base parametersFemale micePGE2 productionHydronephrosisHigher survival rateMiceExcretionSignificant differencesUrinaryMalesSexPossible mechanism