2016
Isoforms of Spectrin and Ankyrin Reflect the Functional Topography of the Mouse Kidney
Stankewich MC, Moeckel GW, Ji L, Ardito T, Morrow JS. Isoforms of Spectrin and Ankyrin Reflect the Functional Topography of the Mouse Kidney. PLOS ONE 2016, 11: e0142687. PMID: 26727517, PMCID: PMC4703142, DOI: 10.1371/journal.pone.0142687.Peer-Reviewed Original ResearchConceptsBowman's capsuleEndothelial cellsFunctional topographyThick ascending loopGlomerular endothelial cellsProximal tubule cellsCapillary endothelial cellsAscending loopDistal tubulesDistal nephronTubule cellsTubular segmentsKidneyRodent kidneyWestern blottingMouse kidneyImmuno-electron microscopyThick loopAnkyrin GMetabolite traffickingSpectrin scaffoldHenleNephronCapsulePodocytes
2011
Increased Tubular Proliferation as an Adaptive Response to Glomerular Albuminuria
Guo JK, Marlier A, Shi H, Shan A, Ardito TA, Du ZP, Kashgarian M, Krause DS, Biemesderfer D, Cantley LG. Increased Tubular Proliferation as an Adaptive Response to Glomerular Albuminuria. Journal Of The American Society Of Nephrology 2011, 23: 429-437. PMID: 22193389, PMCID: PMC3294312, DOI: 10.1681/asn.2011040396.Peer-Reviewed Original ResearchMeSH KeywordsAlbuminuriaAnimalsAxl Receptor Tyrosine KinaseCell ProliferationDisease Models, AnimalFemaleHeparin-binding EGF-like Growth FactorIntegrasesIntercellular Signaling Peptides and ProteinsIntracellular Signaling Peptides and ProteinsKidney GlomerulusKidney Tubules, ProximalMaleMembrane ProteinsMiceMice, TransgenicPodocytesProteinuriaProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesConceptsGlomerular proteinuriaTubular injuryTubular proliferationStructural glomerular injuryProteinuric renal diseaseOnset of albuminuriaRenal tubular atrophyDiphtheria toxin receptorRenal tubular cellsProximal tubule cellsGlomerular albuminuriaRenal failureSystemic inflammationTubular damageProgressive glomerulosclerosisRenal diseaseTubular atrophyGlomerular injuryRenal responsePodocyte lossProliferative responseTubular cellsAnimal modelsProteinuriaReceptor Axl
2010
Inhibition of Podocyte FAK Protects against Proteinuria and Foot Process Effacement
Ma H, Togawa A, Soda K, Zhang J, Lee S, Ma M, Yu Z, Ardito T, Czyzyk J, Diggs L, Joly D, Hatakeyama S, Kawahara E, Holzman L, Guan JL, Ishibe S. Inhibition of Podocyte FAK Protects against Proteinuria and Foot Process Effacement. Journal Of The American Society Of Nephrology 2010, 21: 1145-1156. PMID: 20522532, PMCID: PMC3152231, DOI: 10.1681/asn.2009090991.Peer-Reviewed Original ResearchTargeted deletion of βIII spectrin impairs synaptogenesis and generates ataxic and seizure phenotypes
Stankewich MC, Gwynn B, Ardito T, Ji L, Kim J, Robledo RF, Lux SE, Peters LL, Morrow JS. Targeted deletion of βIII spectrin impairs synaptogenesis and generates ataxic and seizure phenotypes. Proceedings Of The National Academy Of Sciences Of The United States Of America 2010, 107: 6022-6027. PMID: 20231455, PMCID: PMC2851889, DOI: 10.1073/pnas.1001522107.Peer-Reviewed Original ResearchConceptsBetaIII spectrinSpinocerebellar ataxia type 5Spectrin membrane skeletonTargeted gene disruptionAmino acid transportersExcitatory amino acid transportersImpairs synaptogenesisProtein traffickingSeizure disorderGene disruptionDark Purkinje cellsMembrane skeletonAlphaII-spectrinAcid transportersMechanistic basisPurkinje cellsMembrane channelsGlutamate receptor deltaIntracellular pathwaysSpectrin bindsSynaptic proteinsSpectrinReceptor deltaProteinGolgi profiles
2007
The commonly used β-actin-GFP transgenic mouse strain develops a distinct type of glomerulosclerosis
Guo JK, Cheng EC, Wang L, Swenson ES, Ardito TA, Kashgarian M, Cantley LG, Krause DS. The commonly used β-actin-GFP transgenic mouse strain develops a distinct type of glomerulosclerosis. Transgenic Research 2007, 16: 829-834. PMID: 17594530, DOI: 10.1007/s11248-007-9107-x.Peer-Reviewed Original Research
2006
Prevention of mesangial sclerosis by bone marrow transplantation
Guo J, Ardito TA, Kashgarian M, Krause DS. Prevention of mesangial sclerosis by bone marrow transplantation. Kidney International 2006, 70: 910-913. PMID: 16850025, DOI: 10.1038/sj.ki.5001698.Peer-Reviewed Original ResearchConceptsBone marrow transplantationMesangial sclerosisMarrow transplantationUrinary albumin lossSimilar therapeutic effectsOnset of diseaseWild-type BMIntrarenal administrationRenal functionRenal histologyRenal diseaseDisease onsetRenal pathologyBM cellsTherapeutic effectEngraftment levelsRenal cellsAlbumin lossKidney samplesMiceSclerosisTransplantationUntreated controlsDiseaseAdministration
2004
Paracellular Cl- permeability is regulated by WNK4 kinase: Insight into normal physiology and hypertension
Kahle KT, MacGregor GG, Wilson FH, Van Hoek AN, Brown D, Ardito T, Kashgarian M, Giebisch G, Hebert SC, Boulpaep EL, Lifton RP. Paracellular Cl- permeability is regulated by WNK4 kinase: Insight into normal physiology and hypertension. Proceedings Of The National Academy Of Sciences Of The United States Of America 2004, 101: 14877-14882. PMID: 15465913, PMCID: PMC522037, DOI: 10.1073/pnas.0406172101.Peer-Reviewed Original ResearchConceptsPseudohypoaldosteronism type IIPHAII-mutant WNK4Paracellular fluxPotent antihypertensive agentTight junction proteinsTight junctionsAntihypertensive agentsParacellular ion fluxPharmacologic propertiesTight junction structureTranscellular transportersWild-type WNK4Normal physiologyHypertensionTransepithelial resistanceWNK signalingKidney epitheliumTight junction formationParacellular pathwayWNK4Effect of WNK4EpitheliumType IIWNK4 kinaseHomeostasis