2016
Pigment epithelium‐derived factor restoration increases bone mass and improves bone plasticity in a model of osteogenesis imperfecta type VI via Wnt3a blockade
Belinsky GS, Sreekumar B, Andrejecsk JW, Saltzman WM, Gong J, Herzog RI, Lin S, Horsley V, Carpenter TO, Chung C. Pigment epithelium‐derived factor restoration increases bone mass and improves bone plasticity in a model of osteogenesis imperfecta type VI via Wnt3a blockade. The FASEB Journal 2016, 30: 2837-2848. PMID: 27127101, PMCID: PMC4970601, DOI: 10.1096/fj.201500027r.Peer-Reviewed Original ResearchConceptsPigment epithelium-derived factorOsteogenesis imperfecta type VIWnt/β-catenin signalingBone massOI type VIΒ-catenin signalingAbility of PEDFTrabecular bone volume/total volumeType VIBone volume/total volumeWild-type miceEpithelium-derived factorBone plasticityPEDF-knockout miceMesenchymal stem cell commitmentBone volume fractionKO micePEDF peptidesStem cell commitmentFluorescent protein reporterCombination of Wnt3aMouse modelWnt modulatorsBone mineralizationMice
2013
Determination of mesenchymal stem cell fate by pigment epithelium‐derived factor (PEDF) results in increased adiposity and reduced bone mineral content
Gattu AK, Swenson ES, Iwakiri Y, Samuel VT, Troiano N, Berry R, Church CD, Rodeheffer MS, Carpenter TO, Chung C. Determination of mesenchymal stem cell fate by pigment epithelium‐derived factor (PEDF) results in increased adiposity and reduced bone mineral content. The FASEB Journal 2013, 27: 4384-4394. PMID: 23887690, PMCID: PMC3804749, DOI: 10.1096/fj.13-232900.Peer-Reviewed Original ResearchConceptsPigment epithelium-derived factorMesenchymal stem cell fateHuman MSCsMesenchymal stem cell differentiationStem cell fateStem cell differentiationEpithelium-derived factorCell fateOsteogenesis imperfecta type VISignal transductionMSC differentiationNegative regulatorSERPINF1 geneProtein productsOsteoblast differentiationCell differentiationOsteoblast precursorsHuman diseasesPEDF-knockout micePeroxisome proliferator-activated receptorDifferentiation patternsMurine MSCsProliferator-activated receptorAdipocyte markersControl-treated cells
2009
Increased Bone Volume and Correction of HYP Mouse Hypophosphatemia in the Klotho/HYP Mouse
Brownstein CA, Zhang J, Stillman A, Ellis B, Troiano N, Adams DJ, Gundberg CM, Lifton RP, Carpenter TO. Increased Bone Volume and Correction of HYP Mouse Hypophosphatemia in the Klotho/HYP Mouse. Endocrinology 2009, 151: 492-501. PMID: 19952276, PMCID: PMC2817612, DOI: 10.1210/en.2009-0564.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCalciumCrosses, GeneticDNA PrimersDNA-Binding ProteinsFamilial Hypophosphatemic RicketsFemaleFemurFibroblast Growth Factor-23Genetic Diseases, X-LinkedGenotypeGlucuronidaseHeterozygoteHomozygoteHumansKlotho ProteinsMaleMiceMice, KnockoutNuclear ProteinsPolymerase Chain ReactionTibiaTomography, X-Ray ComputedTranscription FactorsConceptsTrabecular bone densityHyp miceBone densityGreater trabecular bone volume fractionFibroblast growth factor 23Serum PTH levelsDihydroxyvitamin D levelsGrowth factor 23Vitamin D metabolismTrabecular bone volume fractionDouble knockout miceKlotho null miceFGF23 effectsKlotho lossPhosphaturic activityPTH levelsFGF23 actionFGF23 levelsBone volume fractionFactor 23D metabolismD levelsFGF receptor 1Osteoid volumeBone volumeNuclear Isoforms of Fibroblast Growth Factor 2 Are Novel Inducers of Hypophosphatemia via Modulation of FGF23 and KLOTHO*
Xiao L, Naganawa T, Lorenzo J, Carpenter TO, Coffin JD, Hurley MM. Nuclear Isoforms of Fibroblast Growth Factor 2 Are Novel Inducers of Hypophosphatemia via Modulation of FGF23 and KLOTHO*. Journal Of Biological Chemistry 2009, 285: 2834-2846. PMID: 19933269, PMCID: PMC2807337, DOI: 10.1074/jbc.m109.030577.Peer-Reviewed Original ResearchAbsorptiometry, PhotonAnimalsCell NucleusFibroblast Growth Factor 2Fibroblast Growth Factor-23Fibroblast Growth FactorsGlucuronidaseHomeostasisHumansHypophosphatemiaIsomerismKidneyKlotho ProteinsMaleMiceMice, TransgenicMolecular WeightOsteoblastsOsteomalaciaPhenotypePhosphatesPromoter Regions, GeneticSkullSodium-Phosphate Cotransporter Proteins, Type IIaX-Ray MicrotomographySurvey of the Enthesopathy of X-Linked Hypophosphatemia and Its Characterization in Hyp Mice
Liang G, Katz LD, Insogna KL, Carpenter TO, Macica CM. Survey of the Enthesopathy of X-Linked Hypophosphatemia and Its Characterization in Hyp Mice. Calcified Tissue International 2009, 85: 235-246. PMID: 19609735, PMCID: PMC2988401, DOI: 10.1007/s00223-009-9270-6.Peer-Reviewed Original ResearchMeSH KeywordsAchilles TendonAdolescentAdultAgedAnimalsBiomarkersCalcinosisChildDisease Models, AnimalDisease ProgressionFamilial Hypophosphatemic RicketsFemaleFibroblast Growth Factor-23Fibroblast Growth FactorsGenetic Diseases, X-LinkedHumansMiceMice, Inbred C57BLMiddle AgedPatellar LigamentPhenotypeQuadriceps MuscleRadiographyRheumatic DiseasesTendinopathyTendonsYoung AdultConceptsFGF-23Fibroblast growth factor receptor 3Hyp miceMajority of patientsHigh circulating levelsPhosphate-regulating hormoneBone spur formationTendon insertion siteGrowth factor receptor 3Insertion siteLigament insertion sitesCirculating LevelsPhosphate excretionBone-forming osteoblastsHeterotopic calcificationOsteophyte formationHistological examinationMurine modelReceptor 3Spur formationHypophosphatemiaEnthesis fibrocartilageBone mineralizationBiochemical milieuMice
2005
Hypophosphatemia leads to rickets by impairing caspase-mediated apoptosis of hypertrophic chondrocytes
Sabbagh Y, Carpenter TO, Demay MB. Hypophosphatemia leads to rickets by impairing caspase-mediated apoptosis of hypertrophic chondrocytes. Proceedings Of The National Academy Of Sciences Of The United States Of America 2005, 102: 9637-9642. PMID: 15976027, PMCID: PMC1172249, DOI: 10.1073/pnas.0502249102.Peer-Reviewed Original ResearchConceptsParathyroid hormone levelsMineral ion homeostasisRachitic changesHormone levelsAbnormal mineral ion homeostasisDihydroxyvitamin D levelsVitamin D deficiencyDegree of hypophosphatemiaHypertrophic chondrocyte layerVitamin D receptorHypertrophic chondrocytesNormal phosphorus levelsGrowth plate maturationD deficiencyD levelsNormal calciumD receptorChondrocyte layerHypophosphatemiaVDR actionChondrocyte apoptosisNull miceRicketsCaspase-mediated apoptosisHypercalcemia
1998
Osteocalcin production in primary osteoblast cultures derived from normal and Hyp mice.
Carpenter T, Moltz K, Ellis B, Andreoli M, McCarthy T, Centrella M, Bryan D, Gundberg C. Osteocalcin production in primary osteoblast cultures derived from normal and Hyp mice. Endocrinology 1998, 139: 35-43. PMID: 9421395, DOI: 10.1210/endo.139.1.5677.Peer-Reviewed Original ResearchConceptsPrimary osteoblast culturesOsteoblast culturesRegulation of osteocalcinMessenger RNAMurine osteoblastsOsteocalcin productionOsteocalcin messenger RNASpecies-specific effectsPrimary murine osteoblastsMaturation-dependent fashionHyp mouse modelHyp miceMutant strainOsteoblast differentiationMurine cellsCultured cellsHYP culturesMurine culturesOsteoblastsRNACell viabilityPrimary culturesRegulationAltered responseNormal litter mates