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 ResearchConceptsKO miceProximal tubulesMouse proximal tubulesWater reabsorptionAcid-base parametersKnockout miceAquaporin 1 knockout miceAquaporin-1Rat kidneyRenal clearance experimentsProximal tubule transportWater channel aquaporin-1Significant differencesHigh urine flowRat proximal tubuleKidney proximal tubulesWT miceUrine flowClearance experimentsGlomerulotubular balanceBlood pHTubule transportAQP1 knockout miceMiceFluid absorption
2021
Sex difference in kidney electrolyte transport III: Impact of low K intake on thiazide-sensitive cation excretion in male and female mice
Xu S, Li J, Yang L, Wang CJ, Liu T, Weinstein AM, Palmer LG, Wang T. Sex difference in kidney electrolyte transport III: Impact of low K intake on thiazide-sensitive cation excretion in male and female mice. Pflügers Archiv - European Journal Of Physiology 2021, 473: 1749-1760. PMID: 34455480, PMCID: PMC8528772, DOI: 10.1007/s00424-021-02611-5.Peer-Reviewed Original ResearchConceptsGlomerular filtration rateFemale miceUrine volumeNaCl cotransporterLow K intakeMeasurement of functionSex differencesNatriuretic responseFractional excretionK intakeTransport protein expressionFiltration rateNCC abundanceNCC expressionRenal clearanceDistal nephronLK dietCation excretionPlasma KNCC proteinNKCC2 expressionWestern blottingProtein expressionMiceFENaRestoration 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- transport
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
2014
Kir1.1 (ROMK) and Kv7.1 (KCNQ1/KvLQT1) are essential for normal gastric acid secretion: importance of functional Kir1.1
Vucic E, Alfadda T, MacGregor GG, Dong K, Wang T, Geibel JP. Kir1.1 (ROMK) and Kv7.1 (KCNQ1/KvLQT1) are essential for normal gastric acid secretion: importance of functional Kir1.1. Pflügers Archiv - European Journal Of Physiology 2014, 467: 1457-1468. PMID: 25127675, DOI: 10.1007/s00424-014-1593-0.Peer-Reviewed Original ResearchConceptsGastric parietal cellsPotassium channelsParietal cellsΒ-subunitKir1.1 channelsWild-type miceSecretagogue-stimulated gastric acid secretionApical poleGastric glandsLeak pathwayPotential therapeutic targetKir1.1Proton secretionRegulatory characteristicsKv7.1Therapeutic targetATPaseCell numberParietal cell numberCellsNormal gastric acid secretionSecretionInhibitorsAcid secretionMice
2013
REGULATION OF GLOMERULOTUBULAR BALANCE IV: IMPLICATION OF AQUAPORIN 1 IN FLOW‐DEPENDENT TRANSPORT AND CELL VOLUME
Du Z, Yan Q, Weinbaum S, Weinstein A, Wang T. REGULATION OF GLOMERULOTUBULAR BALANCE IV: IMPLICATION OF AQUAPORIN 1 IN FLOW‐DEPENDENT TRANSPORT AND CELL VOLUME. The FASEB Journal 2013, 27: 912.27-912.27. DOI: 10.1096/fasebj.27.1_supplement.912.27.Peer-Reviewed Original ResearchKO miceProximal tubulesAQP-1Proximal NaPerfusion rateWT miceFlow-dependent changesCell volumeVolume reabsorptionWater reabsorptionMiceMouse kidneyHCO-3ReabsorptionPeritubular membraneSignificant differencesTubulesAquaporin-1Flow-dependent transportKOH-ATPaseKidneyPrincipal pathwayMicroperfusionPathwayProximal 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 ResearchConceptsKO miceMetabolic acidosisBicarbonate reabsorptionAcid loadNHE3 knockout miceProximal tubule NHE3Mild metabolic acidosisCre transgenic miceExchanger NHE3NH4Cl acid loadMicroperfusion studiesWT miceKnockout miceFloxed miceTransgenic micePathophysiologic statesExcretion rateBicarbonate absorptionNH4Cl loadingMutant miceVolume reabsorptionWestern blotMiceSpecific knockoutAbsorption defect
2012
Genetic modifiers of hypertension in soluble guanylate cyclase α1–deficient mice
Buys ES, Raher MJ, Kirby A, Mohd S, Baron DM, Hayton SR, Tainsh LT, Sips PY, Rauwerdink KM, Yan Q, Tainsh RE, Shakartzi HR, Stevens C, Decaluwé K, da Gloria Rodrigues-Machado M, Malhotra R, Van de Voorde J, Wang T, Brouckaert P, Daly MJ, Bloch KD. 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 SpecificityVasodilationConceptsNitric oxideEndothelium-dependent vasorelaxationOnset of hypertensionVascular smooth muscleNO/cGMPSoluble guanylate cyclaseAdditional genetic factorsAldosterone systemRAAS inhibitionArterial pressureMale miceHypertensionSmooth muscleBlood flowGuanylate cyclaseMouse strainsΑ1 subunitGenetic factorsMiceReceptor componentsGenetic modifiersVasorelaxationRenin
2011
Chloride 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 microscopyGENDER DIFFERENCE IN MODULATION OF ANGIOTENSIN II TYPE 2 RECEPTOR (AT2) FUNCTION AND EXPRESSION IN AT1A RECEPTOR‐DEFICIENT MICE
Yan Q, Wan L, Du Z, Gotoh N, Wang T. GENDER DIFFERENCE IN MODULATION OF ANGIOTENSIN II TYPE 2 RECEPTOR (AT2) FUNCTION AND EXPRESSION IN AT1A RECEPTOR‐DEFICIENT MICE. The FASEB Journal 2011, 25: 835.9-835.9. DOI: 10.1096/fasebj.25.1_supplement.835.9.Peer-Reviewed Original ResearchGlomerular filtration rateUrine volumeAT2 receptorsProximal tubulesAT1A receptor-deficient miceNull miceExpression levelsReceptor-deficient miceKidneys of malesFemale null miceMale null miceAT2 inhibitorNatriuretic effectRenal functionAT2 expressionWT miceFiltration rateBolus injectionReal-time PCRRenal clearancePD123319ENaC expressionReceptor functionMiceReceptors
2010
PSEUDOHYPERKALAEMIA INDUCED BY BLOOD COLLECTION AND CORRECTIONS FOR HEMOLYSIS IN BLOOD SAMPLES FROM EXPERIMENTAL MICE
Yan Q, Du Z, Gotoh N, Giebisch G, Wang T. PSEUDOHYPERKALAEMIA INDUCED BY BLOOD COLLECTION AND CORRECTIONS FOR HEMOLYSIS IN BLOOD SAMPLES FROM EXPERIMENTAL MICE. The FASEB Journal 2010, 24: 1024.3-1024.3. DOI: 10.1096/fasebj.24.1_supplement.1024.3.Peer-Reviewed Original ResearchBlood samplesBlood collection methodBlood collectionCarotid artery cannulationWild-type miceBlood potassium concentrationGenetic backgroundArtery cannulationPlasma potassiumCardiac punctureExperimental micePlasma KHemoglobin concentrationMicePotassium concentrationHemolysisPunctureBleeding methodHemoglobinDifferent genetic backgroundsSimilar genetic backgroundCannulation
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 mechanismMouse model of type II Bartter's syndrome. II. Altered expression of renal sodium- and water-transporting proteins
Wagner CA, Loffing-Cueni D, Yan Q, Schulz N, Fakitsas P, Carrel M, Wang T, Verrey F, Geibel JP, Giebisch G, Hebert SC, Loffing J. Mouse model of type II Bartter's syndrome. II. Altered expression of renal sodium- and water-transporting proteins. American Journal Of Physiology. Renal Physiology 2008, 294: f1373-f1380. PMID: 18322017, DOI: 10.1152/ajprenal.00613.2007.Peer-Reviewed Original ResearchMeSH KeywordsAdaptation, PhysiologicalAnimalsBartter SyndromeCarrier ProteinsCation Transport ProteinsDinoprostoneDisease Models, AnimalEpithelial Sodium ChannelsKidney Tubules, DistalKidney Tubules, ProximalLoop of HenleMiceMice, Mutant StrainsPotassium Channels, Inwardly RectifyingReverse Transcriptase Polymerase Chain ReactionSodiumSodium-Hydrogen Exchanger 3Sodium-Hydrogen ExchangersSodium-Phosphate Cotransporter Proteins, Type IIaSodium-Potassium-Chloride SymportersSolute Carrier Family 12, Member 1Up-RegulationWaterConceptsThick ascending limbBartter's syndromeBartter-like phenotypeType II Bartter's syndromeWild-type miceAntenatal Bartter syndromeWild-type littermatesROMK null micePlasma aldosteroneMaternal polyhydramniosRenal sodiumVolume depletionRenal tubulopathyMouse modelSemiquantitative immunoblottingProximal tubulesAscending limbKidney homogenatesSyndromeHenle's loopNull miceDCT cellsWater transport proteinsCompensatory mechanismsMiceBLOOD PRESSURE AND RENAL FUNCTIONS IN MALE AND FEMALE sEH KNOCKOUT MICE
Yan Q, Raksaseri P, Weldon S, Kabcenell A, Hebert S, Wang T. BLOOD PRESSURE AND RENAL FUNCTIONS IN MALE AND FEMALE sEH KNOCKOUT MICE. The FASEB Journal 2008, 22: 479.34-479.34. DOI: 10.1096/fasebj.22.1_supplement.479.34.Peer-Reviewed Original Research
2007
Blocking angiotensin II type 2 receptor (AT2) induces diuresis and natriuresis in AT1A receptor‐deficient mice
Yan Q, Du Z, Duan Y, Weinbaum S, Weinstein A, Wang T. Blocking angiotensin II type 2 receptor (AT2) induces diuresis and natriuresis in AT1A receptor‐deficient mice. The FASEB Journal 2007, 21: a1246-a1246. DOI: 10.1096/fasebj.21.6.a1246-c.Peer-Reviewed Original ResearchMean arterial blood pressureGlomerular filtration rateAT1A receptor-deficient miceReceptor-deficient miceUrine volumeAT2 receptorsLower mean arterial blood pressureAngiotensin II type 2 receptorAdministration of PD123319Renin-angiotensin systemArterial blood pressureType 2 receptorBlocker PD123319Blood pressureIntravenous bolusFiltration rateKO miceRenal handlingRenal clearancePD123319Receptor functionFluid homeostasisWater handlingReceptorsMice
2004
Renal and intestinal transport defects in Slc26a6-null mice
Wang Z, Wang T, Petrovic S, Tuo B, Riederer B, Barone S, Lorenz JN, Seidler U, Aronson PS, Soleimani M. Renal and intestinal transport defects in Slc26a6-null mice. American Journal Of Physiology - Cell Physiology 2004, 288: c957-c965. PMID: 15574486, DOI: 10.1152/ajpcell.00505.2004.Peer-Reviewed Original ResearchConceptsWild-type miceProximal tubulesSlc26a6-null miceHCO3- secretionKidney proximal tubulesApical membrane ClNull miceBaseline rateNormal blood pressureCl-/formate exchangeBlood pressureKidney functionElectrolyte profileMucosal tissuesIntestinal physiologyUssing chambersSmall intestineMiceFluid absorptionNaCl absorptionStatistical significanceCl-/HCO3NaCl transportDuodenumTubules
2003
ROMK is required for expression of the 70-pS K channel in the thick ascending limb
Lu M, Wang T, Yan Q, Wang W, Giebisch G, Hebert SC. ROMK is required for expression of the 70-pS K channel in the thick ascending limb. American Journal Of Physiology. Renal Physiology 2003, 286: f490-f495. PMID: 14600033, DOI: 10.1152/ajprenal.00305.2003.Peer-Reviewed Original ResearchConceptsThick ascending limbBartter's syndromeK dietK channelsAscending limbChannel activityApical K channelsFunctional expressionHypokalemic alkalosisTAL cellsNull miceSK activityHeterozygous miceHeterogeneous disorderMicePotassium recyclingROMKFunction mutationsSyndromeCritical subunitApical conductanceSalt absorptionLimbDietExpression