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 enlargementSyndrome
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
Olfactory 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
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 injuryPSEUDOHYPERKALAEMIA 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
Mouse 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 mechanismsMice
2006
Maxi-K channels contribute to urinary potassium excretion in the ROMK-deficient mouse model of Type II Bartter's syndrome and in adaptation to a high-K diet
Bailey M, Cantone A, Yan Q, MacGregor G, Leng Q, Amorim J, Wang T, Hebert S, Giebisch G, Malnic G. Maxi-K channels contribute to urinary potassium excretion in the ROMK-deficient mouse model of Type II Bartter's syndrome and in adaptation to a high-K diet. Kidney International 2006, 70: 51-59. PMID: 16710355, DOI: 10.1038/sj.ki.5000388.Peer-Reviewed Original ResearchMeSH KeywordsAdaptation, PhysiologicalAnimalsBartter SyndromeBiological TransportDietDisease Models, AnimalHypokalemiaKidney Tubules, DistalLarge-Conductance Calcium-Activated Potassium ChannelsLoop of HenleMiceMice, Mutant StrainsPeptidesPotassiumPotassium Channels, Inwardly RectifyingPotassium, DietaryConceptsLate distal tubuleType II Bartter's syndromePotassium secretionDistal tubulesPotassium excretionRenal potassiumBartter's syndromeUrinary potassium excretionRenal potassium excretionRenal potassium lossFree-flow micropunctureDistal convoluted tubuleWild-type miceLoop of HenleThick ascending limbSalt-wasting disorderPersistent hypokalemiaMaxi-K channelsMouse modelConvoluted tubulesK secretionStationary microperfusionAscending limbHenle's loopSyndrome
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
Intracellular Na concentration and Rb uptake in proximal convoluted tubule cells and abundance of Na/K-ATPase α1-subunit in NHE3−/− mice
Beck F, Neuhofer W, Dörge A, Giebisch G, Wang T. Intracellular Na concentration and Rb uptake in proximal convoluted tubule cells and abundance of Na/K-ATPase α1-subunit in NHE3−/− mice. Pflügers Archiv - European Journal Of Physiology 2003, 446: 100-105. PMID: 12690468, DOI: 10.1007/s00424-002-1001-z.Peer-Reviewed Original ResearchConceptsIntracellular Na concentrationNa/K-ATPaseΑ1 subunitTubule cellsProximal convoluted tubule cellsDistal convoluted tubuleWild-type miceNa/K-ATPase activityPCT cellsConvoluted tubule cellsIntracellular Cl- concentrationK-ATPaseWestern blot analysisK-ATPase activityNa concentrationRenal cortexCell Na concentrationConvoluted tubulesNa/K-ATPase α1 subunitNa/HNHE3 deficiencyK-ATPase α1-subunitMiceFluid absorption
2000
Defective fluid and HCO3 − absorption in proximal tubule of neuronal nitric oxide synthase-knockout mice
Wang T, Inglis F, Kalb R. Defective fluid and HCO3 − absorption in proximal tubule of neuronal nitric oxide synthase-knockout mice. American Journal Of Physiology. Renal Physiology 2000, 279: f518-f524. PMID: 10966931, DOI: 10.1152/ajprenal.2000.279.3.f518.Peer-Reviewed Original ResearchMeSH KeywordsAcid-Base EquilibriumAnimalsBicarbonatesBiological TransportBlood Gas AnalysisBody FluidsElectrolytesEnzyme InhibitorsInjections, IntravenousKidney Tubules, ProximalMiceMice, Inbred C57BLMice, KnockoutNG-Nitroarginine Methyl EsterNitric Oxide SynthaseNitric Oxide Synthase Type IPotassiumSodiumConceptsWild-type miceNNOS knockout miceL-NAMEProximal tubulesBlood pressureMetabolic acidosisNeuronal nitric oxide synthase knockout miceNitric oxide synthase knockout miceAbsorption of fluidFluid absorptionNeuronal nitric oxide synthaseRenal clearance techniquesMean blood pressureSignificant metabolic acidosisSynthase knockout miceMonomethyl-L-arginine methyl esterNitric oxide synthaseWild-type control animalsProximal tubule transportLuminal perfusion solutionAcid-base balanceIntravenous bolusUrinary excretionUrine volumeClearance technique