Fig. 4.

CST knockout exaggerates OA development in the DMM model. (A) At 4 and 8 weeks, more severe structure loss was present in CST−/− mice than in WT mice as shown through safranin O staining. (B-D) Loss of proteoglycan (arbitrary units) and cartilage thickness (μm) and reduced OARSI scores were detected in CST−/− mice in OA. (E-H) Levels of OA-associated biomarkers MMP-13, ADAMTS-5, iNOS and IL-6 were assayed through Real-time PCR and indicated promotion of CST deficiency. (I) ADAMTS-5 and MMP-13 signals were increased in CST−/− mice, as detected through immunohistochemistry. (J) Increased expression of iNOS was found in CST−/− mice in comparison with WT mice through western blotting. (K) IL-6 was found to be increased in CST−/− mice, as detected by ELISA. (L-N) Col 2, Aggrecan and Sox-9 levels all showed large decreases in CST−/− mice in DMM models through Real-time PCR. (O, P) Col2 was found to decrease greatly in CST−/− mice in DMM models as detected by western blotting (*p < .01). n = 7 for each group, Scale bar: 150 μm.