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Figure 1 | Arthritis Research & Therapy

Figure 1

From: p16INK4a and its regulator miR-24 link senescence and chondrocyte terminal differentiation-associated matrix remodeling in osteoarthritis

Figure 1

Interleukin-1-beta (IL-1β) induces both p16INK4aexpression and a senescence-associated secretory phenotype (SASP) in mature chondrocytes. Osteoarthritis (OA) human primary chondrocytes were placed in pellet culture and treated with IL-1β (10 ng/mL) for 5 days. (A) Aggrecan mRNA (Acan) expression level was evaluated by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) (n = 3). (B) p16INK4a protein expression level was measured by Western blotting. (C) P-p38MAPK protein level was detected by immunohistochemistry (IHC) on a section of paraffin-embedded pellets. Images were taken with a ×20 objective. (D- G) Matrix metalloprotease 1 (MMP1), MMP13, IL-6, and IL-8 secretion were measured by enzyme-linked immunosorbent assay (ELISA) (n = 4). Data are shown as mean ± standard deviation (SD) of fold changes compared with control. *P <0.05, **P <0.01.

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