2011
Actin and ERK1/2-CEBPβ signaling mediates phagocytosis-induced innate immune response of osteoprogenitor cells
Lee HG, Minematsu H, Kim KO, Aydemir A, Shin MJ, Nizami SA, Chung KJ, Hsu AC, Jacobs CR, Lee FY. Actin and ERK1/2-CEBPβ signaling mediates phagocytosis-induced innate immune response of osteoprogenitor cells. Biomaterials 2011, 32: 9197-9206. PMID: 21899882, PMCID: PMC3193180, DOI: 10.1016/j.biomaterials.2011.08.059.Peer-Reviewed Original ResearchMeSH KeywordsActinsAdhesivenessAnimalsBenzimidazolesBone and BonesCCAAT-Enhancer-Binding Protein-betaCyclooxygenase 2Cytochalasin DExtracellular Signal-Regulated MAP KinasesGene Expression RegulationHumansImmunity, InnateInflammationInterleukin-6MAP Kinase Signaling SystemMiceModels, BiologicalOsteogenesisOsteolysisPhagocytosisProtein Kinase InhibitorsSignal TransductionSkullStem CellsTime FactorsTitaniumConceptsInflammatory osteolysisInflammatory responseMacrophage-mediated inflammatory responsesKey inflammatory pathwaysSuitable therapeutic targetInflammatory gene expressionInnate immune responseOsteoprogenitor cellsInflammatory cascadeInflammatory pathwaysImmune responseTherapeutic targetHost bone-implant interfaceAZD6244 treatmentIntracellular mechanismsBone-implant interfaceBone formationCellular mechanismsERK pathwayInflammationΒ pathwayOsteoclastogenesisOsteolysisIntracellular signalingImplant osteointegrationNuclear 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
Targeting extracellular signal-regulated kinase (ERK) signaling has therapeutic implications for inflammatory osteolysis
Seo SW, Lee D, Minematsu H, Kim AD, Shin M, Cho SK, Kim DW, Yang J, Lee FY. Targeting extracellular signal-regulated kinase (ERK) signaling has therapeutic implications for inflammatory osteolysis. Bone 2009, 46: 695-702. PMID: 19895919, PMCID: PMC2823832, DOI: 10.1016/j.bone.2009.10.032.Peer-Reviewed Original ResearchConceptsInflammatory osteolysisInflammatory responseInnate immune responseExtracellular signal-regulated kinase (ERK) signalingImportant therapeutic targetM-CSF expressionSignal-regulated kinase 1/2 pathwaySignal-regulated kinase signalingExtracellular signal-regulated kinase 1/2 (ERK1/2) pathwayInhibition of ERKImmune responseTherapeutic implicationsTherapeutic targetOsteoclast precursorsKinase 1/2 pathwayM-CSFOsteolysisERK pathwayMacrophage colonyLPSERKERK signalsMitogen-activated protein kinase (MAPK) familyKinase signalingCell differentiation