Figure 2

FGF8 induced the decrease in the sulfated glycosaminoglycan content in the cellular matrix. Chondrocytes were treated without (none) or with 100 ng/ml FGF8 and/or 0.01 ng/ml IL-1α and various concentrations of anti-FGF8 antibody (Ab) for 48 hours. Sulfated glycosaminoglycan (S-GAG) content of the residual cellular matrix was measured using the 1,9-dimethylmethylene blue method. Each column represents the mean ± standard error. (a) FGF8 induced S-GAG degradation, which was concentration-dependently inhibited by anti-FGF8 antibody (1, 3 and 10 μg/ml). Representative data of three independent experiments. ^$$$P < 0.001 compared with the no treatment group (Student's t test), ***P < 0.001 compared with FGF8 alone (Dunnett test). (b) Chondrocytes were treated with IL-1α (IL-1), FGF8, or IL-1α with FGF8 (IL-1 + FGF8). IL-1α enhanced FGF8-induced S-GAG degradation (IL-1 + FGF8). Anti-FGF8 antibody (1, 3 and 10 μg/ml) concentration-dependently inhibited that degradation by FGF8 with IL-1α. Data from a single experiment are shown, but similar data were obtained in two additional experiments. ^###P < 0.001 compared with the no treatment group (Student's t test), ⁺⁺P < 0.01 compared with IL-1α alone (Aspin–Welch test), ^&&P < 0.01 compared with FGF8 alone (Student's t test), **P < 0.01 and ***P < 0.001 compared with the IL-1α + FGF8-treated group (Dunnett test).