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Influence of Glucocorticoids on Cellular Senescence Hallmarks in Osteoarthritic Fibroblast-like Synoviocytes
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he following are available online at https://www.mdpi.com/article/10.3390/jcm10225331/s1, Figure S1: Influence of prednisolone on DNA damage in osteoarthriticfibroblast-like synoviocytes (cells recovering after 8 days); Figure S2: Influence of prednisolone onsenescence hallmarks in osteoarthritic fibroblast-like synoviocytes (cells recovering after 15 days);Figure S3: Influence of prednisolone on DNA damage in irradiated osteoarthritic fibroblast-likesynoviocytes (cells recovering after 8 days); Figure S4: Influence of prednisolone on DNA damagein mesenchymal stem cells; Figure S5: Influence of prednisolone on DNA damage in irradiatedosteoarthritic fibroblast-like synoviocytes (cells re-covering after 8 days). Representative picturesof DNA damage with ÈH2AX staining; Figure S6: Influence of prednisolone on DNA damage inmesenchymal stem cells. Representative pictures of DNA damage with ÈH2AX staining.. International audience. Osteoarthritis (OA) is recognized as being a cellular senescence-linked disease. Intra-articular injections of glucocorticoids (GC) are frequently used in knee OA to treat synovial effusion but face controversies about toxicity. We investigated the influence of GC on cellular senescence hallmarks and senescence induction in fibroblast-like synoviocytes (FLS) from OA patients and mesenchymal stem cells (MSC). Methods: Cellular senescence was assessed via the proliferation rate, β-galactosidase staining, DNA damage and CKI expression (p21, p16INK4A). Experimental senescence was induced by irradiation. Results: The GC prednisolone did not induce an apparent senescence phenotype in FLS, with even higher proliferation, no accumulation of β-galactosidase-positive cells nor DNA damage and reduction in p21mRNA, only showing the enhancement of p16INK4A. Prednisolone did not modify experimental senescence induction in FLS, with no modulation of any senescence parameters. Moreover, prednisolone did not induce a senescence phenotype in MSC: despite high β-galactosidase-positive cells, no reduction in proliferation, no DNA damage and no CKI enhancement was observed. Conclusions: We provide reassuring in vitro data about the use of GC regarding cellular senescence involvement in OA: the GC prednisolone did not induce a senescent phenotype in OA FLS (the proliferation ratio was even higher) and in MSC and did not worsen cellular senescence establishment.
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