2016
Loss of Cystic Fibrosis Transmembrane Regulator Impairs Intestinal Oxalate Secretion
Knauf F, Thomson RB, Heneghan JF, Jiang Z, Adebamiro A, Thomson CL, Barone C, Asplin JR, Egan ME, Alper SL, Aronson PS. Loss of Cystic Fibrosis Transmembrane Regulator Impairs Intestinal Oxalate Secretion. Journal Of The American Society Of Nephrology 2016, 28: 242-249. PMID: 27313231, PMCID: PMC5198290, DOI: 10.1681/asn.2016030279.Peer-Reviewed Original ResearchConceptsIntestinal oxalate secretionWild-type miceCystic fibrosisIntestinal tissueOxalate secretionIncidence of hyperoxaluriaCalcium oxalate stone formationNet intestinal absorptionOxalate stone formationCoexpression of CFTRIntestinal transport processesWestern blot analysisOxalate absorptionMouse modelIntestinal absorptionGlucose absorptionUssing chambersStone formationFibrosisMiceSecretionReduced expressionCystic fibrosis transmembrane conductance regulator (CFTR) geneHyperoxaluriaPatients
2012
Sat1 is dispensable for active oxalate secretion in mouse duodenum
Ko N, Knauf F, Jiang Z, Markovich D, Aronson PS. Sat1 is dispensable for active oxalate secretion in mouse duodenum. American Journal Of Physiology - Cell Physiology 2012, 303: c52-c57. PMID: 22517357, PMCID: PMC3404526, DOI: 10.1152/ajpcell.00385.2011.Peer-Reviewed Original ResearchConceptsCalcium oxalate stonesMouse duodenumOxalate secretionOxalate stonesIntestinal oxalate secretionIntestinal oxalate transportSecretory fluxSAT1 expressionDisulfonic stilbene DIDSDuodenumTransporter 1SecretionMiceHyperoxalemiaBasolateral solutionHyperoxaluriaBasolateral transportersBicarbonate productionOxalate transportBasolateral membraneSAT1Apical membraneComplete removalMedium concentration
2010
Role of SLC26A6-mediated Cl⁻-oxalate exchange in renal physiology and pathophysiology.
Aronson PS. Role of SLC26A6-mediated Cl⁻-oxalate exchange in renal physiology and pathophysiology. Journal Of Nephrology 2010, 23 Suppl 16: s158-64. PMID: 21170874.Commentaries, Editorials and LettersConceptsNull miceCalcium oxalate urolithiasisProximal tubule cellsStone riskAnimal modelsOxalate urolithiasisProximal tubulesOxalate homeostasisTubule cellsApical membrane ClHyperoxaluriaRenal physiologyOxalate exchangeMiceExchange activitySubsequent studiesAnion transportersPossible mechanismHyperoxalemiaPatientsPathophysiologyUrolithiasisStriking phenotypeReabsorption
2008
Phenotypic and Functional Analysis of Human SLC26A6 Variants in Patients With Familial Hyperoxaluria and Calcium Oxalate Nephrolithiasis
Monico CG, Weinstein A, Jiang Z, Rohlinger AL, Cogal AG, Bjornson BB, Olson JB, Bergstralh EJ, Milliner DS, Aronson PS. Phenotypic and Functional Analysis of Human SLC26A6 Variants in Patients With Familial Hyperoxaluria and Calcium Oxalate Nephrolithiasis. American Journal Of Kidney Diseases 2008, 52: 1096-1103. PMID: 18951670, PMCID: PMC2710965, DOI: 10.1053/j.ajkd.2008.07.041.Peer-Reviewed Original ResearchConceptsPrimary hyperoxaluria type 1Oxalate transportMajor risk factorCalcium oxalate nephrolithiasisUrine oxalate levelsCalcium oxalate urolithiasisRare variantsHyperoxaluria type 1Calcium oxalate stonesAdditional missense variantsUrine oxalateOxalate excretionRisk factorsOxalate nephrolithiasisOxalate urolithiasisHyperoxaluriaAbstractTextAdult subjectsType 1Oxalate stonesPotential modifiersStudy designOxalate levelsGood healthMissense variants
2007
Role of Anion Transporter SLC26A6 (CFEX) in Prevention of Hyperoxaluria and Urolithiasis
Aronson P. Role of Anion Transporter SLC26A6 (CFEX) in Prevention of Hyperoxaluria and Urolithiasis. AIP Conference Proceedings 2007, 900: 141-148. DOI: 10.1063/1.2723570.Commentaries, Editorials and LettersProximal tubulesNull miceOxalate secretionPlasma oxalate concentrationIntestinal oxalate secretionCalcium oxalate urolithiasisFormate exchangeOxalate exchangePrevention of hyperoxaluriaHigh incidenceOxalate urolithiasisHyperoxaluriaCFEXApical membraneRenal brush border vesiclesNet absorptionMiceBrush border vesiclesTubulesUrolithiasisSecretionXenopus oocytesAnion transportersFunctional expression
2006
Calcium oxalate urolithiasis in mice lacking anion transporter Slc26a6
Jiang Z, Asplin JR, Evan AP, Rajendran VM, Velazquez H, Nottoli TP, Binder HJ, Aronson PS. Calcium oxalate urolithiasis in mice lacking anion transporter Slc26a6. Nature Genetics 2006, 38: 474-478. PMID: 16532010, DOI: 10.1038/ng1762.Peer-Reviewed Original ResearchConceptsCalcium oxalate urolithiasisOxalate urolithiasisPlasma oxalate concentrationIntestinal oxalate secretionUrinary oxalate concentrationCommon urologic diseaseNet intestinal absorptionAnion exchanger SLC26A6Dietary oxalate restrictionSlc26a6-null miceSignificant hyperoxaluriaOxalate restrictionUrologic diseasesHigh incidenceIntestinal absorptionExchanger SLC26A6Mutant miceUrolithiasisMiceMajor constitutive roleNet absorptionOxalate secretionHyperoxaluriaOxalate concentrationEpithelial tissues