2017
Response of Npt2a knockout mice to dietary calcium and phosphorus
Li Y, Caballero D, Ponsetto J, Chen A, Zhu C, Guo J, Demay M, Jüppner H, Bergwitz C. Response of Npt2a knockout mice to dietary calcium and phosphorus. PLOS ONE 2017, 12: e0176232. PMID: 28448530, PMCID: PMC5407772, DOI: 10.1371/journal.pone.0176232.Peer-Reviewed Original ResearchConceptsCompared to WT miceWT miceDietary calciumDietary phosphateCalcium x phosphorus productUrine phosphate levelsUrinary calcium excretionUrine anion gapDevelopment of novel therapiesWild-typeRenal stone diseaseWild-type miceNpt2a-knockout (KO) miceCalcium excretionFGF23 levelsNovel therapiesPreventing nephrolithiasisPlasma phosphateStone diseaseAnion gapAddition of calciumKnockout micePhosphorus productCalcium phosphate depositionHuman carriers
2016
Hypophosphatemia promotes lower rates of muscle ATP synthesis
Pesta DH, Tsirigotis DN, Befroy DE, Caballero D, Jurczak MJ, Rahimi Y, Cline GW, Dufour S, Birkenfeld AL, Rothman DL, Carpenter TO, Insogna K, Petersen KF, Bergwitz C, Shulman GI. Hypophosphatemia promotes lower rates of muscle ATP synthesis. The FASEB Journal 2016, 30: 3378-3387. PMID: 27338702, PMCID: PMC5024687, DOI: 10.1096/fj.201600473r.Peer-Reviewed Original ResearchConceptsMuscle ATP synthesisATP synthesisMuscle weaknessIsolated muscle mitochondriaSolute carrier familyWild-type littermate controlsSolute carrier family 34Carrier familyLower ratesInsulin-stimulated ratesMuscle mitochondriaChronic hypophosphatemiaHeart failureHypophosphatemic groupHypophosphatemic miceHypophosphatemiaLittermate controlsKnockout miceBlood PLow ratePlasma PPatientsSimilar findingsMember 1Plasma inorganic phosphate
2010
Acute Down-regulation of Sodium-dependent Phosphate Transporter NPT2a Involves Predominantly the cAMP/PKA Pathway as Revealed by Signaling-selective Parathyroid Hormone Analogs
Nagai S, Okazaki M, Segawa H, Bergwitz C, Dean T, Potts JT, Mahon MJ, Gardella TJ, Jüppner H. Acute Down-regulation of Sodium-dependent Phosphate Transporter NPT2a Involves Predominantly the cAMP/PKA Pathway as Revealed by Signaling-selective Parathyroid Hormone Analogs. Journal Of Biological Chemistry 2010, 286: 1618-1626. PMID: 21047792, PMCID: PMC3020770, DOI: 10.1074/jbc.m110.198416.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCattleChlorocebus aethiopsCOS CellsCyclic AMPCyclic AMP-Dependent Protein KinasesDown-RegulationHumansIn Vitro TechniquesKidney Tubules, ProximalMaleMiceMice, Inbred C57BLOpossumsOsteoblastsParathyroid HormonePhosphorusPseudohypoparathyroidismRatsSignal TransductionSodiumSodium-Phosphate Cotransporter Proteins, Type IIaConceptsAcute down-regulationNpt2a expressionParathyroid hormoneRenal proximal tubule cellsParathyroid hormone (PTH)/PTH-related peptideCAMP/PKALong-acting PTH analogPTH analogsWild-type miceRenal proximal tubulesIntracellular calcium responsesParathyroid hormone analogProximal tubule cellsOpossum kidney cellsM-PTH(1Prolonged cAMP responsesParathyroid hormone analoguesCAMP/PKA signaling pathwayPTH-dependent regulationRenal brush border membraneClonal cell linesInducing IP(3Pseudohypoparathyroid patientsMembrane expressionCalcium response
2008
Cellular Mechanism of Decreased Bone in Brtl Mouse Model of OI: Imbalance of Decreased Osteoblast Function and Increased Osteoclasts and Their Precursors*
Uveges TE, Collin‐Osdoby P, Cabral WA, Ledgard F, Goldberg L, Bergwitz C, Forlino A, Osdoby P, Gronowicz GA, Marini JC. Cellular Mechanism of Decreased Bone in Brtl Mouse Model of OI: Imbalance of Decreased Osteoblast Function and Increased Osteoclasts and Their Precursors*. Journal Of Bone And Mineral Research 2008, 23: 1983-1994. PMID: 18684089, PMCID: PMC2686922, DOI: 10.1359/jbmr.080804.Peer-Reviewed Original ResearchConceptsColony-forming unitsRANKL/OPG ratioOsteogenesis imperfectaWildtype valuesCompared to wildtype miceSevere osteogenesis imperfectaReal-time RT-PCRMouse model of OIIncreases osteoclast precursorsBone-resorbing osteoclastsOI therapyKnock-in modelIncreased osteoclastsOsteoclast increaseMarrow culturesWildtype miceModel of OITRACP stainingOsteoblast functionOsteoclast precursorsCellular mechanismsBrtl miceOsteoclastsRT-PCRTRACP(+Genetic Evidence of Serum Phosphate-Independent Functions of FGF-23 on Bone
Sitara D, Kim S, Razzaque MS, Bergwitz C, Taguchi T, Schüler C, Erben RG, Lanske B. Genetic Evidence of Serum Phosphate-Independent Functions of FGF-23 on Bone. PLOS Genetics 2008, 4: e1000154. PMID: 18688277, PMCID: PMC2483943, DOI: 10.1371/journal.pgen.1000154.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBone and BonesBone DensityCalcification, PhysiologicCells, CulturedFibroblast Growth Factor-23Fibroblast Growth FactorsGene ExpressionHypophosphatemiaMiceMice, Inbred C57BLMice, KnockoutMuscle, SkeletalOsteoblastsPhenotypePhosphatesSerumSkullSodium-Phosphate Cotransporter Proteins, Type IIaUrineConceptsFGF-23 geneFgf-23-/- micePhosphate homeostasisGenetic evidenceFgf-23-/-Regulation of phosphate homeostasisCrucial biological importanceFirst genetic evidenceSystemic phosphate homeostasisSkeletal mineralizationCellular functionsDouble mutantNew mouse lineMaster regulatorProtein abundanceGenomic ablationMolecular mechanismsDouble mutant miceChondrocyte differentiationTargeted disruptionSkeletal phenotypeBiological importanceGenesEnergy metabolismHomeostasis