2017
Calreticulin inhibits inflammation‐induced osteoclastogenesis and bone resorption
Fischer CR, Mikami M, Minematsu H, Nizami S, Lee H, Stamer D, Patel N, Soung D, Back JH, Song L, Drissi H, Lee FY. Calreticulin inhibits inflammation‐induced osteoclastogenesis and bone resorption. Journal Of Orthopaedic Research® 2017, 35: 2658-2666. PMID: 28460421, PMCID: PMC8996436, DOI: 10.1002/jor.23587.Peer-Reviewed Original ResearchConceptsRecombinant human calreticulinIntracellular proteinsCalcium-binding chaperoneDifferent cell typesRecombinant formTranscription factorsFusion of monocytesExtracellular functionsNew therapeutic opportunitiesK activityCathepsin K activityCell typesCalreticulinCytoplasmic 1Anti-osteoclastogenic effectPrecursor cellsMetastatic bone cancerFactor 1Human calreticulinActivated T cellsOsteoclast precursor cellsProteinNuclear factorC-fosMouse calvarial bones
2015
CA‐074Me compound inhibits osteoclastogenesis via suppression of the NFATc1 and c‐FOS signaling pathways
Patel N, Nizami S, Song L, Mikami M, Hsu A, Hickernell T, Chandhanayingyong C, Rho S, Compton JT, Caldwell J, Kaiser PB, Bai H, Lee HG, Fischer CR, Lee FY. CA‐074Me compound inhibits osteoclastogenesis via suppression of the NFATc1 and c‐FOS signaling pathways. Journal Of Orthopaedic Research® 2015, 33: 1474-1486. PMID: 25428830, DOI: 10.1002/jor.22795.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCathepsin BDipeptidesMaleMAP Kinase Signaling SystemMice, Inbred C57BLNFATC Transcription FactorsNF-kappa BOsteoclastsProto-Oncogene Proteins c-fosRANK LigandConceptsOsteolytic disordersOsteoclast biologyBone resorptionCA-074MeC-FOSMechanisms of cathepsinsCathepsin B knockout miceB knockout miceCathepsin B inhibitor CA-074Dose-dependent mannerOsteoclast resorption pitsCathepsin B inhibitionInhibits osteoclastogenesisNFATc1 pathwayNew therapiesOsteoclastogenic effectsCA-074Knockout miceLysosomal proteasesMature osteoclastsResorption pitsCathepsin KNew targetsOsteoclastsCompound inhibits
2011
Nuclear presence of nuclear factor of activated T cells (NFAT) c3 and c4 is required for Toll-like receptor-activated innate inflammatory response of monocytes/macrophages
Minematsu H, Shin MJ, Aydemir A, Kim KO, Nizami SA, Chung GJ, Lee FY. Nuclear presence of nuclear factor of activated T cells (NFAT) c3 and c4 is required for Toll-like receptor-activated innate inflammatory response of monocytes/macrophages. Cellular Signalling 2011, 23: 1785-1793. PMID: 21726630, PMCID: PMC3169434, DOI: 10.1016/j.cellsig.2011.06.013.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBone MarrowCell NucleusChromatin ImmunoprecipitationCytokinesHumansImmunity, InnateImmunohistochemistryLipopeptidesLipopolysaccharidesMacrophagesMiceMice, KnockoutMonocytesNFATC Transcription FactorsNF-kappa BOligopeptidesPrimary Cell CultureRNA Polymerase IIRNA, MessengerSignal TransductionToll-Like ReceptorsTumor Necrosis Factor-alphaConceptsBone marrow-derived macrophagesInnate immune responseImmune responseLPS stimulationNuclear factorNFAT-luciferase reporterProinflammatory cytokine expressionInnate inflammatory responseTLR ligand stimulationToll-like receptorsActivated T cells c3Monocytes/macrophagesActivated T cellsInnate immune regulationRole of NFATsTNF mRNA expressionMarrow-derived macrophagesImmune regulatory proteinsTLR4 ligandCytokine expressionLess TNFTLR1/2 ligandInflammatory responseImmune regulationT cells
2009
Nuclear factor of activated T cells mediates fluid shear stress- and tensile strain-induced Cox2 in human and murine bone cells
Aydemir A, Minematsu H, Gardner TR, Kim KO, Ahn JM, Lee FY. Nuclear factor of activated T cells mediates fluid shear stress- and tensile strain-induced Cox2 in human and murine bone cells. Bone 2009, 46: 167-175. PMID: 19748606, PMCID: PMC2818272, DOI: 10.1016/j.bone.2009.08.061.Peer-Reviewed Original ResearchConceptsActivated T cellsT cellsBone cellsMechanical stimulationNuclear factorPathways of inflammationCytokine gene inductionMouse bone cellsMurine bone cellsBone massCOX2 inductionCOX2 expressionStability of implantsCalvarial bone cellsOsseous integrationHost boneNuclear translocationFluid shear stressDaily activitiesStimulationTranscription factorsNovel roleImplantsNFAT2Osteoblastic lineage
2007
Orthopedic Implant Particle‐Induced Tumor Necrosis Factor‐α Production in Macrophage–Monocyte Lineage Cells Is Mediated by Nuclear Factor of Activated T Cells
MINEMATSU H, SHIN MJ, AYDEMIR A, SEO SW, KIM DW, BLAINE TA, MACIÁN F, YANG J, LEE F. Orthopedic Implant Particle‐Induced Tumor Necrosis Factor‐α Production in Macrophage–Monocyte Lineage Cells Is Mediated by Nuclear Factor of Activated T Cells. Annals Of The New York Academy Of Sciences 2007, 1117: 143-150. PMID: 18056040, DOI: 10.1196/annals.1402.026.Peer-Reviewed Original ResearchConceptsActivated T cellsT cellsLineage cellsTumor Necrosis Factor-α ProductionNuclear factorMonocyte-macrophage lineage cellsTNF-alpha protein secretionTNF-alpha expressionTNF-alpha productionTNF-alpha gene expressionTumor necrosis factorMurine macrophage-like RAW264.7Macrophage-like RAW264.7TNF-alpha inductionMonocyte-macrophage cellsTNF-alphaNecrosis factorSpecific molecular mechanismsImplant particlesJoint prosthesesMolecular mechanismsNuclear Factor of Activated T Cell Mediates Proinflammatory Gene Expression in Response to Mechanotransduction
AYDEMIR A, LEE S, KIM D, GARDNER TR, PRINCE D, AHN J, LEE F. Nuclear Factor of Activated T Cell Mediates Proinflammatory Gene Expression in Response to Mechanotransduction. Annals Of The New York Academy Of Sciences 2007, 1117: 138-142. PMID: 17584983, DOI: 10.1196/annals.1402.004.Peer-Reviewed Original Research