Journal: Cell Proliferation

Article Title: Aspirin reverses inflammatory suppression of chondrogenesis by stabilizing YAP

doi: 10.1111/cpr.13380

Figure Lengend Snippet: Aspirin reverses TNF‐α‐inhibited chondrogenic markers expression during chondrogenesis of BMMSCs. (A, B) Relative mRNA and protein expression levels of chondrogenic markers (COL2A1, ACAN, and SOX9) were measured in BMMSCs treated with or without TNF‐α and aspirin for 7 days by qRT‐PCR and western blot analyses, respectively. (C, D) Relative mRNA and protein expression levels of chondrogenic markers (COL2A1, ACAN, and SOX9) were measured in BMMSCs treated with or without TNF‐α and aspirin for 14 days by qRT‐PCR and western blot analyses, respectively. (E, F) Relative mRNA and protein expression levels of chondrogenic markers (COL2A1, ACAN, and SOX9) were measured in BMMSCs treated with or without TNF‐α and aspirin for 21 days by qRT‐PCR and western blot analyses, respectively. (G) IHC staining of COL2A1 in cartilage pellets cultured under different treatment conditions for 7, 14, and 21 days. (H) Quantification of the COL2A1 IHC staining data. Data in (A), (C), (E), and (H) are given as the mean ± SD of three independent experiments. ACAN, aggrecan; COL2A1, collagen type II alpha 1 chain; GAPDH, glyceraldehyde‐3‐phosphate dehydrogenase; SOX9, SRY‐box transcription factor 9. * p < 0.05, ** p < 0.01, *** p < 0.001. Scale bars: 250 μm

Article Snippet: Pellets were cultured in the Mesenchymal Stem Cell Chondrogenic Differentiation Medium (#7551, ScienCell, USA) with or without TNF‐α (10 ng/ml) and AS (100 μM) for 7, 14, and 21 days.

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Immunohistochemistry, Cell Culture

Journal: Cell Proliferation

Article Title: Aspirin reverses inflammatory suppression of chondrogenesis by stabilizing YAP

doi: 10.1111/cpr.13380

Figure Lengend Snippet: Aspirin mitigates the progression of cartilage degeneration in a mouse DMM model. A schematic of the in vivo experiment. After DMM surgery, mice were injected with aspirin or PBS for 12 weeks ( n = 10 per group). (B) The body weights of mice from different treatment groups were measured after 12 weeks. (C) Representative H&E and safranin O‐fast green staining images of the left knee joint of mice after exposure to different treatments for 8 weeks ( n = 5 per group). (D) The severity of the OA‐like phenotype 8 weeks after DMM surgery in (C) was analysed by the Osteoarthritis Research Society International (OARSI) score system. (E) Representative H&E and safranin O‐fast green staining images of the left knee joint of mice after exposure to different treatments for 12 weeks ( n = 5 per group). (F) The severity of the OA‐like phenotype 12 weeks after DMM surgery in (E) was analysed by the Osteoarthritis Research Society International (OARSI) score system. (G) IHC staining of chondrogenic markers (COL2A1 and SOX9) and catabolic markers (MMP9 and MMP13) in the left knee joint of mice after different treatments for 8 weeks. (H) IHC staining scores of (G). (I) IHC staining of chondrogenic markers (COL2A1 and SOX9) and catabolic markers (MMP9 and MMP13) in the left knee joint of mice after different treatments for 12 weeks. (J) IHC staining scores of (I). COL2A1, collagen type II alpha 1 chain; MMP9, matrix metallopeptidase 9; MMP13, matrix metallopeptidase 13; SOX9, SRY‐box transcription factor 9. * p < 0.05, ** p < 0.01, *** p < 0.001. Scale bars: 0.5 mm (50× figures), 250 μm (100× figures), 100 μm (200× figures), 50 μm (400× figures)

Article Snippet: Pellets were cultured in the Mesenchymal Stem Cell Chondrogenic Differentiation Medium (#7551, ScienCell, USA) with or without TNF‐α (10 ng/ml) and AS (100 μM) for 7, 14, and 21 days.

Techniques: In Vivo, Injection, Staining, Immunohistochemistry