2019
Bladder urothelial BK channel activity is a critical mediator for innate immune response in urinary tract infection pathogenesis
Yeh J, Lu M, Alvarez-Lugo L, Chai TC. Bladder urothelial BK channel activity is a critical mediator for innate immune response in urinary tract infection pathogenesis. American Journal Of Physiology. Renal Physiology 2019, 316: f617-f623. PMID: 30648906, DOI: 10.1152/ajprenal.00554.2018.Peer-Reviewed Original ResearchConceptsUrinary tract infectionInnate immune responseImmune responseBK channel activityUrinary tract infection pathogenesisChannel activityFemale C57BL/6 miceInflammatory protein-2Voltage-gated potassium channelsUropathogenic Escherichia coliInhibitor iberiotoxinUPEC exposureUTI pathogenesisInflammatory biomarkersTract infectionsC57BL/6 miceIL-6Urinary biomarkersUrinary changesBiomarker levelsInfection pathogenesisUrine specimensProtein 10LPS inoculationSame biomarkers
2018
Mouse urothelial genes associated with voiding behavior changes after ovariectomy and bladder lipopolysaccharide exposure
Acevedo‐Alvarez M, Yeh J, Alvarez‐Lugo L, Lu M, Sukumar N, Hill WG, Chai TC. Mouse urothelial genes associated with voiding behavior changes after ovariectomy and bladder lipopolysaccharide exposure. Neurourology And Urodynamics 2018, 37: 2398-2405. PMID: 29682797, DOI: 10.1002/nau.23592.Peer-Reviewed Original ResearchConceptsUrinary tract infectionOveractive bladderOVX miceVoiding behaviorFemale C57BL6/J miceC57BL6/J micePost-menopausal womenEffects of ovariectomyBehavior changeMicturition changesTransurethral instillationLPS instillationTract infectionsSham surgeryLPS exposureJ miceCOX-2OVX surgeryDay 1Day 3Consecutive daysSurgeryMiceSpot assayGene expression changesLipopolysaccharide stimulates BK channel activity in bladder umbrella cells
Lu M, Li JR, Alvarez-Lugo L, Li Y, Yu S, Li X, Shi B, Chai TC. Lipopolysaccharide stimulates BK channel activity in bladder umbrella cells. American Journal Of Physiology - Cell Physiology 2018, 314: c643-c653. PMID: 29466671, DOI: 10.1152/ajpcell.00339.2017.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCyclic AMP-Dependent Protein KinasesFemaleLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsLipopolysaccharide ReceptorsLipopolysaccharidesLymphocyte Antigen 96Membrane PotentialsMice, Inbred C57BLPatch-Clamp TechniquesPotassiumSignal TransductionToll-Like Receptor 4Urinary BladderUrinary Tract InfectionsUrotheliumConceptsBK channel activityBK channelsChannel activityUmbrella cellsUrinary tract infectionFemale C57BL6 micePotassium channel inhibitorsUropathogenic Escherichia coliProtein kinase ATract infectionsLPS effectsC57BL6 miceBladder urotheliumLamina propriaMin of exposureChannel inhibitorsBacterial infectionsLPS receptorUrothelial tissuesUrothelial cellsUrotheliumLipopolysaccharidePotassium channelsRT-PCRPKA blocker
2016
Granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) is released by female mouse bladder urothelial cells and expressed by the urothelium as an early response to lipopolysaccharides (LPS)
Li Y, Lu M, Alvarez‐Lugo L, Chen G, Chai TC. Granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) is released by female mouse bladder urothelial cells and expressed by the urothelium as an early response to lipopolysaccharides (LPS). Neurourology And Urodynamics 2016, 36: 1020-1025. PMID: 27337494, DOI: 10.1002/nau.23057.Peer-Reviewed Original ResearchConceptsBladder urotheliumCyclooxygenase-2GM-CSFCyclooxygenase-1GM-CSFRαBladder tissueMRNA expressionTumor necrosis factor αCOX-2 mRNA expressionVivo LPS exposureVascular endothelial growth factorNecrosis factor αDose-dependent releaseIncrease of VEGFGranulocyte-macrophage colony-stimulating factor (GM-CSF) signalingBladder urothelial cellsConcentrations of lipopolysaccharideGM-CSF mRNA expressionEndothelial growth factorGM-CSF antibodyMouse bladder urotheliumGM-CSF activityLPS exposurePain transductionSingle dose
2010
Mouse cystic fibrosis transmembrane conductance regulator forms cAMP-PKA–regulated apical chloride channels in cortical collecting duct
Lu M, Dong K, Egan ME, Giebisch GH, Boulpaep EL, Hebert SC. Mouse cystic fibrosis transmembrane conductance regulator forms cAMP-PKA–regulated apical chloride channels in cortical collecting duct. Proceedings Of The National Academy Of Sciences Of The United States Of America 2010, 107: 6082-6087. PMID: 20231442, PMCID: PMC2851921, DOI: 10.1073/pnas.0902661107.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBenzoatesChloride ChannelsCyclic AMPCyclic AMP-Dependent Protein KinasesCystic Fibrosis Transmembrane Conductance RegulatorFemaleIn Vitro TechniquesKidney CortexKidney Tubules, CollectingKineticsMiceMice, Inbred C57BLMice, Inbred CFTRMice, KnockoutMice, TransgenicMutationOocytesPatch-Clamp TechniquesPotassium Channels, Inwardly RectifyingRecombinant ProteinsThiazolidinesXenopus laevisConceptsCystic fibrosis transmembrane conductance regulatorFibrosis transmembrane conductance regulatorTransmembrane conductance regulatorCl- channel activityConductance regulatorCl- channelsApical membrane proteinsExpression of CFTRChannel activityCFTR Cl- channelApical chloride channelApical cell membraneDeltaF508 CFTR mutationMembrane proteinsCatalytic subunitXenopus laevis oocytesForm proteinPrincipal cellsCFTR channelsROMK null miceApical patchesApical membraneSingle-channel conductanceChloride channelsCell membrane
2006
CFTR is required for PKA-regulated ATP sensitivity of Kir1.1 potassium channels in mouse kidney
Lu M, Leng Q, Egan ME, Caplan MJ, Boulpaep EL, Giebisch GH, Hebert SC. CFTR is required for PKA-regulated ATP sensitivity of Kir1.1 potassium channels in mouse kidney. Journal Of Clinical Investigation 2006, 116: 797-807. PMID: 16470247, PMCID: PMC1361349, DOI: 10.1172/jci26961.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphateAnimalsCurcuminCyclic AMP-Dependent Protein KinasesCystic Fibrosis Transmembrane Conductance RegulatorHydrogen-Ion ConcentrationKidneyMiceMice, Inbred C57BLMice, Inbred CFTRMice, TransgenicMutationOocytesPatch-Clamp TechniquesPotassium Channels, Inwardly RectifyingXenopus laevisConceptsFunctional switchCystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channelATP sensitivityEffects of CFTRThick ascending limbPotential physiological rolePKA activityRenal K channelsCystic fibrosisPhysiological roleSecretory channelsK channelsRenal tubule epithelial cellsApical membraneCFTRDeltaF508 mutationDistal nephron segmentsCl- channelsK homeostasisTubule epithelial cellsEpithelial cellsTAL cellsPotassium channelsK handlingGlibenclamide sensitivity
2000
Extracellular Atp Inhibits the Small-Conductance K Channel on the Apical Membrane of the Cortical Collecting Duct from Mouse Kidney
Lu M, MacGregor G, Wang W, Giebisch G. Extracellular Atp Inhibits the Small-Conductance K Channel on the Apical Membrane of the Cortical Collecting Duct from Mouse Kidney. The Journal Of General Physiology 2000, 116: 299-310. PMID: 10919872, PMCID: PMC2229488, DOI: 10.1085/jgp.116.2.299.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphateAffinity LabelsAlkaloidsAnimalsCarbazolesColforsinCyclic AMPCyclic AMP-Dependent Protein KinasesCyclic GMP-Dependent Protein KinasesEnzyme InhibitorsExtracellular SpaceIndolesIon Channel GatingKidney Tubules, CollectingMembrane PotentialsMiceMice, Inbred C57BLNaphthalenesNG-Nitroarginine Methyl EsterOkadaic AcidPatch-Clamp TechniquesPhosphoprotein PhosphatasesPhosphorylationPotassiumPotassium ChannelsPotassium Channels, Calcium-ActivatedProtein KinasesRatsRats, Sprague-DawleyReceptors, PurinergicSmall-Conductance Calcium-Activated Potassium ChannelsThionucleotidesUridine TriphosphateConceptsApical membraneChannel activityProtein kinase AProtein kinase C.Protein phosphatasePurinergic receptor stimulationSmall-conductance potassium channelsOkadaic acidExtracellular ATP concentrationKinase AKinase C.Addition of ATPG proteinsRat homologuePhospholipase CPhosphatase activitySK activitySmall-conductance K channelsApical receptorsATP inhibitsSingle-channel analysisATPNucleotide sensitivityApical K channelsK channels