2024
Long-term second-generation antipsychotics decreases bone formation and resorption in male patients with schizophrenia
Wang F, Li H, Yi K, Wu Y, Bian Q, Guo B, Luo X, Kang Y, Wu Q, Ma Q. Long-term second-generation antipsychotics decreases bone formation and resorption in male patients with schizophrenia. Psychopharmacology 2024, 241: 1771-1780. PMID: 38647696, DOI: 10.1007/s00213-024-06592-y.Peer-Reviewed Original ResearchConceptsSecond-generation antipsychoticsBone turnover biomarkersEffects of antipsychoticsInteraction effect of groupCTX-1Effect of groupMale patientsBone fragilityBone resorptionC-terminal telopeptide of type I collagenSGA treatmentFasting peripheral blood samplesTelopeptide of type I collagenSchizophreniaIncreased risk of bone fragilityChinese male patientAntipsychoticsC-terminal telopeptideBalance of bone metabolismRisk of bone fragilityBone formationBalance of bone formationChronic patientsTime-dependent mannerCTX-1 concentrations
2023
Genetics of Diffuse Idiopathic Skeletal Hyperostosis and Ossification of the Spinal Ligaments
Kato H, Braddock D, Ito N. Genetics of Diffuse Idiopathic Skeletal Hyperostosis and Ossification of the Spinal Ligaments. Current Osteoporosis Reports 2023, 21: 552-566. PMID: 37530996, PMCID: PMC10543536, DOI: 10.1007/s11914-023-00814-6.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsDiffuse idiopathic skeletal hyperostosisAutosomal recessive hypophosphatemic rickets type 2Idiopathic skeletal hyperostosisSkeletal hyperostosisOPLL patientsGenetic factorsPathogenic variantsFibroblast growth factor 23Growth factor 23Posterior longitudinal ligamentSpinal ligament ossificationRecent FindingsRecent studiesStrong genetic factorImportant new biomarkerDisease courseFactor 23Longitudinal ligamentClinical evaluationPlasma biomarkersClinical trialsLigament ossificationPlasma PPiCalcification disordersPatientsEctopic calcificationSingle‐Cell Transcriptomics of Bone Marrow Stromal Cells in Diversity Outbred Mice: A Model for Population‐Level scRNA‐Seq Studies
Dillard L, Rosenow W, Calabrese G, Mesner L, Al‐Barghouthi B, Abood A, Farber E, Onengut‐Gumuscu S, Tommasini S, Horowitz M, Rosen C, Yao L, Qin L, Farber C. Single‐Cell Transcriptomics of Bone Marrow Stromal Cells in Diversity Outbred Mice: A Model for Population‐Level scRNA‐Seq Studies. Journal Of Bone And Mineral Research 2023, 38: 1350-1363. PMID: 37436066, PMCID: PMC10528806, DOI: 10.1002/jbmr.4882.Peer-Reviewed Original ResearchConceptsGene regulatory networksMesenchymal lineage cellsBone marrow-derived stromal cellsGenome-wide association studiesOsteocyte-like cellsLineage cellsOsteogenic conditionsTranscriptomic profilesSingle-cell RNA-seqCell typesTranscriptomic data setsGenetics of osteoporosisDisease-Associated VariantsSingle-cell levelMarrow-derived stromal cellsTranscriptomic perspectiveRegulatory networksCausal genesRNA-seqTranscriptomic dataScRNA-seqMesenchymal progenitorsAssociation studiesGenetic studiesLineage precursorsMultifocal heterotopic ossification in a man with germline variants of LIM Mineralization Protein‐1 (LMP‐1)
Sangadala S, Shore E, Xu M, Bergwitz C, Lozano‐Calderon S, Lin A, Boden S, Kaplan F. Multifocal heterotopic ossification in a man with germline variants of LIM Mineralization Protein‐1 (LMP‐1). American Journal Of Medical Genetics Part A 2023, 191: 2164-2174. PMID: 37218523, DOI: 10.1002/ajmg.a.63304.Peer-Reviewed Original ResearchConceptsLIM mineralization protein-1Bone morphogenetic protein (BMP) pathwayGermline variantsBone morphogenetic proteinRecombinant BMP-2LMP-1Gene-disease relationshipsC2C12 cellsGenetic analysisIntracellular proteinsWT proteinHeterotopic ossificationProtein pathwayOsteoblast markersWT cellsBMP-2Protein 1Coding variantsGene-diseaseProtein levelsControl cellsPathogenic variantsLMP-1 variantsCo-transfectionMC3T3 cellsTunable Mesoscopic Collagen Island Architectures Modulate Stem Cell Behavior
Nguyen R, Cabral A, Rossello‐Martinez A, Zulli A, Gong X, Zhang Q, Yan J, Mak M. Tunable Mesoscopic Collagen Island Architectures Modulate Stem Cell Behavior. Advanced Materials 2023, 35: e2207882. PMID: 36895051, PMCID: PMC10166061, DOI: 10.1002/adma.202207882.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell DifferentiationCollagenHydrogelsMammalsMesenchymal Stem CellsOsteogenesisTissue EngineeringConceptsStem cell behaviorCell behaviorPluripotent stem cellsMesenchymal stem cell behaviorMammalian cellsMesodermal differentiationCell migrationExtracellular matrixStem cellsOsteogenic differentiationRegional enrichmentCollagen-based hydrogelsPhysiological tissuesBioactive cuesDifferentiationBiophysical environmentCollagen hydrogelsCellsIslandsComplex architectureTissue engineering applicationsTissueCollagen architectureEnrichmentGelPathogenic mechanisms of glucocorticoid-induced osteoporosis
Chen M, Fu W, Xu H, Liu C. Pathogenic mechanisms of glucocorticoid-induced osteoporosis. Cytokine & Growth Factor Reviews 2023, 70: 54-66. PMID: 36906448, PMCID: PMC10518688, DOI: 10.1016/j.cytogfr.2023.03.002.Peer-Reviewed Original ResearchConceptsGlucocorticoid-induced osteoporosisExogenous glucocorticoidsGC excessBone cellsBone formationImpaired bone formationMultiple adverse effectsLong-term useExcessive glucocorticoidsAutoimmune diseasesBone resorptionPrescribed medicinesEnhanced osteoclastogenesisPathogenic mechanismsProcess of osteoblastogenesisGlucocorticoidsHigh dosesOsteoclast apoptosisApoptosis of osteoblastsMature osteoclastsAdverse effectsOsteoclastsDifferentiation of osteoblastsOsteoporosisOsteoclastogenesis
2022
Vitamin C epigenetically controls osteogenesis and bone mineralization
Thaler R, Khani F, Sturmlechner I, Dehghani SS, Denbeigh JM, Zhou X, Pichurin O, Dudakovic A, Jerez SS, Zhong J, Lee JH, Natarajan R, Kalajzic I, Jiang YH, Deyle DR, Paschalis EP, Misof BM, Ordog T, van Wijnen AJ. Vitamin C epigenetically controls osteogenesis and bone mineralization. Nature Communications 2022, 13: 5883. PMID: 36202795, PMCID: PMC9537512, DOI: 10.1038/s41467-022-32915-8.Peer-Reviewed Original ResearchConceptsSevere skeletal defectsBone-specific genesEpigenetic functionsChromatin accessibilityHistone demethylationDNA hydroxymethylationTranscriptional activityPro-osteogenic genesCell differentiationOsteogenic cell differentiationOsteogenic differentiationGenesSkeletal defectsBone phenotypeMurine boneOsteoblastogenesisDifferentiationKnockout miceGulo knockout miceVitamin C deficiencyTET1Collagen maturationPromoterDemethylationVitamin CInhibitory Effect of Biotransformed-Fucoidan on the Differentiation of Osteoclasts Induced by Receptor for Activation of Nuclear Factor-κB Ligand
Park B, Yu S, Kim S, Lee J, Choi S, Chang J, Yang E, Kim K, Ahn S. Inhibitory Effect of Biotransformed-Fucoidan on the Differentiation of Osteoclasts Induced by Receptor for Activation of Nuclear Factor-κB Ligand. Journal Of Microbiology And Biotechnology 2022, 32: 1017-1025. PMID: 35879294, PMCID: PMC9628933, DOI: 10.4014/jmb.2203.03001.Peer-Reviewed Original ResearchConceptsNuclear factor-κB ligandBone marrow macrophagesOsteoclast differentiationBone homeostasisBackground of osteoporosisLow molecular weight fucoidanExpression of NFATc1Effect of fucoidanDifferentiation of osteoclastsResistant acid phosphatase activityHarmful side effectsSide effectsPharmaceutical treatmentWeight fucoidanKey transcriptional factorOsteoporosisMarrow macrophagesDifferentiated osteoclastsInhibitory effectOsteoclastsRT-PCRC-fosSafe natural product
2021
Selenoprotein W ensures physiological bone remodeling by preventing hyperactivity of osteoclasts
Kim H, Lee K, Kim J, Kim M, Kim J, Lee H, Chung Y, Shin H, Kim T, Park E, Rho J, Lee S, Kim N, Lee S, Choi Y, Jeong D. Selenoprotein W ensures physiological bone remodeling by preventing hyperactivity of osteoclasts. Nature Communications 2021, 12: 2258. PMID: 33859201, PMCID: PMC8050258, DOI: 10.1038/s41467-021-22565-7.Peer-Reviewed Original ResearchConceptsSelenoprotein WCell-cell fusionRNA sequencing analysisProfile of receptor activationOsteoclast differentiationNuclear factor of activated T cells cytoplasmic 1Bone remodelingBone mass phenotypeOsteoclastogenesis in vitroNuclear translocation of NF-kBTranslocation of NF-kBPhysiological bone remodelingBlocks osteoporosisNuclear translocationNuclear factorOsteoclastogenic genesMechanism of actionMass phenotypeBone metabolismBone resorptionReceptor activationOsteoclast maturationCytoplasmic 1Osteoclast formationNF-kBSelective deletion of the receptor for CSF1, c-fms, in osteoclasts results in a high bone mass phenotype, smaller osteoclasts in vivo and an impaired response to an anabolic PTH regimen
Zhu M, Sun BH, Nevius E, Kaplan J, Pereira J, Insogna K. Selective deletion of the receptor for CSF1, c-fms, in osteoclasts results in a high bone mass phenotype, smaller osteoclasts in vivo and an impaired response to an anabolic PTH regimen. PLOS ONE 2021, 16: e0247199. PMID: 33607650, PMCID: PMC7895546, DOI: 10.1371/journal.pone.0247199.Peer-Reviewed Original ResearchConceptsColony stimulating factor 1Mature osteoclastsBone massHigh bone mass phenotypeAttenuated anabolic responseDaily subcutaneous dosesTrabecular bone massBone mass phenotypeC-fmsNormal tooth eruptionTrabecular bone compartmentsMature osteoclast functionCathepsin K promoterFemurs of maleWild-type animalsOcS/BSFemale knockSubcutaneous dosesNormal weightSmall osteoclastsImpaired responseTrabecular numberAnabolic responseFlox miceMass phenotypeProgranulin promotes bone fracture healing via TNFR pathways in mice with type 2 diabetes mellitus
Ding Y, Wei J, Hettinghouse A, Li G, Li X, Einhorn T, Liu C. Progranulin promotes bone fracture healing via TNFR pathways in mice with type 2 diabetes mellitus. Annals Of The New York Academy Of Sciences 2021, 1490: 77-89. PMID: 33543485, PMCID: PMC8138780, DOI: 10.1111/nyas.14568.Peer-Reviewed Original ResearchConceptsType 2 diabetes mellitusRole of progranulinBone fracture healingFracture healingDiabetes mellitusT2DM modelType 1 diabetic conditionAnti-inflammatory activityTranscription-polymerase chain reactionLocal administrationBone marrow cellsExogenous progranulinMKR micePGRN effectsPrimary bone marrow cellsFracture riskDiabetic conditionsPGRN mRNABone fragilityImmunohistochemical stainingMetabolic disordersRecombinant progranulinBone fracturesProgranulinTherapeutic potential
2020
In Vitro Physical and Functional Interaction Assays to Examine the Binding of Progranulin Derivative Atsttrin to TNFR2 and Its Anti-TNFα Activity
Fu W, Hettinghouse A, Liu C. In Vitro Physical and Functional Interaction Assays to Examine the Binding of Progranulin Derivative Atsttrin to TNFR2 and Its Anti-TNFα Activity. Methods In Molecular Biology 2020, 2248: 109-119. PMID: 33185871, PMCID: PMC8112733, DOI: 10.1007/978-1-0716-1130-2_8.Peer-Reviewed Original ResearchConceptsAnti-TNFα activityAutoimmune diseasesTartrate-resistant acid phosphatase (TRAP) stainingAnti-TNFα therapyCollagen-induced arthritisInflammatory disease modelsGood therapeutic effectAcid phosphatase stainingGrowth factor-like moleculesTNF inhibitorsTherapeutic effectTNFα activityProgranulinFunctional inhibitionTNFR2AtsttrinDisease modelsPhosphatase stainingTNFRTNFαDiseaseInhibitionCritical roleDirect bindingHigh affinityBone Marrow and Adipose Tissue Adenosine Receptors Effect on Osteogenesis and Adipogenesis
Eisenstein A, Chitalia S, Ravid K. Bone Marrow and Adipose Tissue Adenosine Receptors Effect on Osteogenesis and Adipogenesis. International Journal Of Molecular Sciences 2020, 21: 7470. PMID: 33050467, PMCID: PMC7589187, DOI: 10.3390/ijms21207470.Peer-Reviewed Original ResearchConceptsBone healthBone marrowPotential therapeutic targetInhibitory receptorsMetabolic disturbancesReceptor effectsTherapeutic implicationsTherapeutic targetMetabolic diseasesEndogenous ligandDichotomous effectsReceptorsMarrowAdenosineAdipogenesisExpression profilesCellular stressHealthOsteogenesisCurrent understandingDifferent tissuesObesityInflammationDiseasePhylogeny and chemistry of biological mineral transport
Schlesinger PH, Braddock DT, Larrouture QC, Ray EC, Riazanski V, Nelson DJ, Tourkova IL, Blair HC. Phylogeny and chemistry of biological mineral transport. Bone 2020, 141: 115621. PMID: 32858255, PMCID: PMC7771281, DOI: 10.1016/j.bone.2020.115621.Peer-Reviewed Original ResearchConceptsImportant evolutionary relationshipsTissue-nonspecific alkaline phosphataseJawless fishEvolutionary relationshipsMineral accumulationKey biological elementsCellular organizationNonspecific alkaline phosphataseCross-linked collagen fibrilsMembrane vesiclesMineral transportSkeletal elementsAmorphous aggregatesDefinitive stageBone physiologyHigh expressionTooth formationMetabolic featuresEpithelial transportMacrophages Promote Aortic Valve Cell Calcification and Alter STAT3 Splicing
Raddatz M, Huffstater T, Bersi M, Reinfeld B, Madden M, Booton S, Rathmell W, Rathmell J, Lindman B, Madhur M, Merryman W. Macrophages Promote Aortic Valve Cell Calcification and Alter STAT3 Splicing. Arteriosclerosis Thrombosis And Vascular Biology 2020, 40: e153-e165. PMID: 32295422, PMCID: PMC7285853, DOI: 10.1161/atvbaha.120.314360.Peer-Reviewed Original ResearchConceptsValve cellsMurine aortic valvesAortic valve diseaseCalcific aortic valve diseaseBone marrow genotypeOsteogenic calcificationAortic valve cellsMacrophage-driven inflammationValve diseaseMacrophage maturationMacrophage recruitmentMacrophage interactionsCell secretionCell calcificationAortic valveTherapeutic targetSTAT3Flow cytometryExpression of MHCIIMaturationBone marrow transplantRecruitmentGenotypesMacrophagesCellsA cut above (and below): Protein cleavage in the regulation of polycystin trafficking and signaling
Padovano V, Mistry K, Merrick D, Gresko N, Caplan MJ. A cut above (and below): Protein cleavage in the regulation of polycystin trafficking and signaling. Cellular Signalling 2020, 72: 109634. PMID: 32283256, PMCID: PMC7269866, DOI: 10.1016/j.cellsig.2020.109634.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell AdhesionHumansOsteogenesisProtein TransportProteolysisSignal TransductionTRPP Cation ChannelsConceptsPolycystin-1Polycystin proteinsG proteinsPolycystin-1 proteinProtein maturationTerminal tailObligate stepBiological pathwaysProtein cleavagePhysiological functionsProteolytic siteProteinPathological consequencesAutosomal dominant polycystic kidney diseaseTraffickingDominant polycystic kidney diseasePolycystic kidney diseasePrimary functionCleavageRegulationMaturationGenesMitochondriaValuable insightsPathway
2019
Impaired ATM activation in B cells is associated with bone resorption in rheumatoid arthritis
Mensah KA, Chen JW, Schickel JN, Isnardi I, Yamakawa N, Vega-Loza A, Anolik JH, Gatti RA, Gelfand EW, Montgomery RR, Horowitz MC, Craft JE, Meffre E. Impaired ATM activation in B cells is associated with bone resorption in rheumatoid arthritis. Science Translational Medicine 2019, 11 PMID: 31748230, PMCID: PMC7167286, DOI: 10.1126/scitranslmed.aaw4626.Peer-Reviewed Original ResearchConceptsRheumatoid arthritisB cellsHealthy donor controlsGroup of patientsHumanized mouse modelImmature B cellsGene segment usageErosive diseaseRA pathophysiologyBone erosionBone lossBone resorptionHigh prevalenceRANKL productionBone densityMouse modelReceptor activatorBone marrowPatientsDonor controlsCD21Segment usageArthritisElevated frequencyAtaxia telangiectasiaBurosumab Improved Histomorphometric Measures of Osteomalacia in Adults with X‐Linked Hypophosphatemia: A Phase 3, Single‐Arm, International Trial
Insogna KL, Rauch F, Kamenický P, Ito N, Kubota T, Nakamura A, Zhang L, Mealiffe M, San Martin J, Portale AA. Burosumab Improved Histomorphometric Measures of Osteomalacia in Adults with X‐Linked Hypophosphatemia: A Phase 3, Single‐Arm, International Trial. Journal Of Bone And Mineral Research 2019, 34: 2183-2191. PMID: 31369697, PMCID: PMC6916280, DOI: 10.1002/jbmr.3843.Peer-Reviewed Original ResearchConceptsAdverse eventsWeek 48Fracture healingMore treatment-emergent adverse eventsTreatment-emergent adverse eventsProcedure-related adverse eventsOsteoid volume/bone volumeMost adverse eventsSerious adverse eventsTransiliac bone biopsiesSerum phosphorus concentrationPoor bone qualityRenal phosphate reabsorptionHuman monoclonal antibodyBone painPersistent osteomalaciaSubcutaneous burosumabPrimary endpointSkeletal complicationsAtraumatic fracturesChronic hypophosphatemiaSerum phosphorusDihydroxyvitamin DBone turnoverBone biopsyCathepsin K-deficient osteocytes prevent lactation-induced bone loss and parathyroid hormone suppression
Lotinun S, Ishihara Y, Nagano K, Kiviranta R, Carpentier VT, Neff L, Parkman V, Ide N, Hu D, Dann P, Brooks D, Bouxsein ML, Wysolmerski J, Gori F, Baron R. Cathepsin K-deficient osteocytes prevent lactation-induced bone loss and parathyroid hormone suppression. Journal Of Clinical Investigation 2019, 129: 3058-3071. PMID: 31112135, PMCID: PMC6668688, DOI: 10.1172/jci122936.Peer-Reviewed Original ResearchConceptsLactation-induced bone lossParathyroid hormoneBone lossBone resorptionCathepsin KMilk calcium levelsParathyroid hormone suppressionSerum parathyroid hormoneRegulation of PTHOsteoclastic bone resorptionTrabecular bone volumeOsteocyte lacunar areaHormone suppressionHigh calcium demandOsteoclast numberCortical thicknessEffect of lactationCalcium levelsNormal rangeBone volumeCalcium demandExact mechanismLacunar areaResorptionSufficient calcium
2018
Polycystin-1 regulates bone development through an interaction with the transcriptional coactivator TAZ
Merrick D, Mistry K, Wu J, Gresko N, Baggs JE, Hogenesch JB, Sun Z, Caplan MJ. Polycystin-1 regulates bone development through an interaction with the transcriptional coactivator TAZ. Human Molecular Genetics 2018, 28: 16-30. PMID: 30215740, PMCID: PMC6298236, DOI: 10.1093/hmg/ddy322.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBone DevelopmentCell DifferentiationE1A-Associated p300 ProteinGene Expression RegulationGenes, RegulatorHEK293 CellsHumansIntracellular Signaling Peptides and ProteinsKidneyModels, AnimalMorpholinosOsteoblastsOsteogenesisPolycystic Kidney, Autosomal DominantTrans-ActivatorsTranscription FactorsTranscriptional Coactivator with PDZ-Binding Motif ProteinsTRPP Cation ChannelsZebrafishZebrafish ProteinsConceptsC-terminal tailCurly tail phenotypePolycystin-1Tail phenotypeTranscriptional coactivator TAZMessenger RNARunx2 transcriptional activityBone developmentTranscription factor Runx2Co-regulatory proteinsPkd1 mutant miceEssential coactivatorTranscriptional pathwaysTranscriptional activityOsteoblast differentiationKey mechanistic linkTAZPhysiological functionsPKD1 geneMechanistic linkRunx2MorpholinoPhenotypeMutant miceAutosomal dominant polycystic kidney disease
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