Aging · 2020 · 27 citations · 35 references
MedicineCell BiologyOrthopaedic SurgeryApoptosisCartilage RepairInflammationArticular Cartilage StructureCartilage BiologyCartilage BreakdownCartilage DegenerationCartilage InjuriesCartilage MetabolismArticular Cartilage LossCartilage Breakdown PathophysiologyCartilage Degradation MechanismsCartilage PhenotypingChondrocyte Phenotype MaintenanceInflammatory Mediators In CartilageOsteoarthritic Cartilage DegenerationOxidative Stress In Cartilage
. CLU knockdown in OA chondrocytes was also performed and its effect on proliferation, hypertrophic phenotype, apoptosis, inflammation and oxidative stress was investigated. CLU expression was upregulated in human OA cartilage and in cultured OA cartilage-derived chondrocytes compared with control group. CLU knockdown reduced cell proliferation and increased hypertrophic phenotype as well as apoptotic death. CLU-silenced OA chondrocytes showed higher MMP13 and COL10A1 as well as greater TNF-α, Nox4 and ROS levels. Our results indicate a possible cytoprotective role of CLU in OA chondrocytes promoting cell survival by its anti-apoptotic, anti-inflammatory and antioxidant properties and counteracting the hypertrophic phenotypic shift. Further studies are needed to deepen the role of CLU in order to identify a new potential therapeutic target for OA.
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Radiological Assessment of Osteo-Arthrosis
Jan Kellgren, J. S. Lawrence · Annals of the Rheumatic Diseases · 1957 · 12.4K citations · Full text