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
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 ResearchAQP-1Proximal tubulesKO miceWild-typeMicroperfused in vitroTransepithelial osmotic gradientHCO-3 transportWT miceNo significant differencePeritubular transportHCO-3 absorptionVolume reabsorptionPeritubular membraneWater reabsorptionAquaporin-1Mouse kidneyMicePerfusion rateH-ATPaseSignificant differenceTubulesReabsorptionOsmotic gradientCell volumePerfusion
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
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 microscopy
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 Research
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 mechanismsMiceThe olfactory isoform of adenylyl cyclase (AC3) in the renal macula densa serves as a key regulator of glomerular filtration rate
Pluznick J, Zou D, Zhang X, Yan Q, Rodriguez‐Gil D, Eisner C, Wells E, Greer C, Schnermann J, Wang T, Firestein S, Caplan M. The olfactory isoform of adenylyl cyclase (AC3) in the renal macula densa serves as a key regulator of glomerular filtration rate. The FASEB Journal 2008, 22: 761.12-761.12. DOI: 10.1096/fasebj.22.1_supplement.761.12.Peer-Reviewed Original ResearchGlomerular filtration rateMacula densaTubuloglomerular feedbackFiltration rateEfferent arteriolar diametersRT-PCRPlasma renin concentrationRenal function studiesAdenylyl cyclaseWild-type littermatesOlfactory G-proteinOlfactory receptorsRenin concentrationRenin secretionArteriolar diameterOlfactory adenylyl cyclaseWestern blotMouse kidneyKidneyNon-olfactory tissuesRenal epitheliumG proteinsFunction studiesMiceKey regulatorBLOOD 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
Functional Expression of Key Components of the Olfactory Receptor Signaling Pathway in the Distal Nephron
Pluznick J, Zhang X, Zou D, Yan Q, Wells E, Wang T, Firestein S, Caplan M. Functional Expression of Key Components of the Olfactory Receptor Signaling Pathway in the Distal Nephron. The FASEB Journal 2007, 21: a500-a500. DOI: 10.1096/fasebj.21.5.a500.Peer-Reviewed Original ResearchGlomerular filtration rateMouse kidneyRenal function studiesMacula densa cellsWild-type littermatesNormal mouse kidneyOlfactory G-proteinOlfactory receptorsReceptor Signaling PathwayRenal functionFiltration rateDistal tubulesDistal nephronKidneyWestern blotTubule segmentsRT-PCRAdenylyl cyclaseMiceNon-olfactory tissuesPotential roleG proteinsSignaling pathwaysFunction studiesMD cells
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 transportDuodenumTubulesMechanosensory function of microvilli of the kidney proximal tubule
Du Z, Duan Y, Yan Q, Weinstein A, Weinbaum S, Wang T. Mechanosensory function of microvilli of the kidney proximal tubule. Proceedings Of The National Academy Of Sciences Of The United States Of America 2004, 101: 13068-13073. PMID: 15319475, PMCID: PMC516518, DOI: 10.1073/pnas.0405179101.Peer-Reviewed Original ResearchConceptsKidney proximal tubulesProximal tubulesNa+ reabsorptionNa+ transportNa+-H+ exchange activityProximal tubule Na+ reabsorptionNa+-H+ exchangeLuminal cell membraneMechanosensory functionNa+ absorptionTubular diameterLuminal diameterMouse kidneyEpithelial microvilliReabsorptionTubulesKidneyAutoregulatory mechanismNa+ uptakeHormonal systemsMiceActin cytoskeletonCell membraneTerminal webBending moment