Skip to main content

Advertisement

Figure 5 | Arthritis Research & Therapy

Figure 5

From: Loss of sclerostin promotes osteoarthritis in mice via β-catenin-dependent and -independent Wnt pathways

Figure 5

Sclerostin preserves anabolic–catabolic balance by inhibiting chondrocyte catabolism and hypertrophy. (A) β-galactosidase assay in TOPGAL chondrocytes (n = 3). Ct, Threshold cycle. (B) Western blot analysis of nuclear proteins showing inhibition of the translocation of β-catenin to the nucleus by sclerostin (Scl) treatment (n = 3). (C) Sclerostin partially restored the expression of the anabolic markers (COL2A1, ACAN and SOX9) (n = 6). (D) Wnt3a-inhibited proteoglycan release by chondrocytes was restored with sclerostin treatment (n = 6). (E) Sclerostin abolished the Wnt3a-increased gene expression of catabolic markers (ADAMTS4, ADAMTS5, MMP3 and MMP13) (n = 5). (F) and (G) Sclerostin abolished the Wnt3a-increased expression of hypertrophic markers (COL10A1 and VEGF (n = 8). (H) Western blot analysis of sclerostin-inhibited expression of Adamts-4 and Adamts-5 and type X collagen (n = 3). (I) Quantification of Alcian Blue staining showing that Wnt3a reduced the accumulation of highly sulfated glycosaminoglycans (GAGs) (n = 5). Wild-type (WT) chondrocytes were used for all the experiments. Data are mean ± SEM. *P < 0.05 versus control; £P < 0.05 versus Wnt3a.

Back to article page