Wif-1 is expressed at cartilage-mesenchyme interfaces and impedes Wnt3a-mediated inhibition of chondrogenesis

Abstract

Supplementary material available online at

Association between Wnt inhibitory factor-1 expression levels in articular cartilage and the disease severity of patients with osteoarthritis of the knee

“…The results of the present study demonstrated that WIF-1 expression is predominantly detected in the superficial layers of articular cartilage. These results are consistent with previous studies which have demonstrated that WIF-1 is highly expressed in the superficial layers of epiphyseal cartilage in bone and tendons (11,12,18). Since WIF-1 is predominantly expressed in articular cartilage, and in bone to a lesser extent (12,18), the present study aimed to investigate whether WIF-1 is upregulated in patients with OA.…”

“…A previous study demonstrated specific binding of WIF-1 to Wnt3a, Wnt4, Wnt5a, Wnt7a, Wnt9a and Wnt11 (18). Furthermore, it has been demonstrated that WIF-1 is capable of blocking Wnt3a-mediated activation of the canonical Wnt signalling pathway, which is associated with cartilage degeneration (18). The results of another previous study demonstrated that WIF-1 was capable of attenuating the CTGF-dependent induction of cartilage matrix gene expression, including aggrecan and COL2A1, in primary murine chondrocytes (11).…”

“…These results suggested that the loss of WIF-1 expression may be an early event in the OA disease progress and indicated that WIF-1 may be associated with the pathogenesis of OA. A previous study demonstrated specific binding of WIF-1 to Wnt3a, Wnt4, Wnt5a, Wnt7a, Wnt9a and Wnt11 (18). Furthermore, it has been demonstrated that WIF-1 is capable of blocking Wnt3a-mediated activation of the canonical Wnt signalling pathway, which is associated with cartilage degeneration (18).…”

Fibroblast Growth Factor Ligand Dependent Proliferation and Chondrogenic Differentiation of Synovium-Derived Stem Cells and Concomitant Adaptation of Wnt/Mitogen-Activated Protein Kinase Signals

“…41 This notion seems well supported by other studies, which suggest that Wnt3a can prevent or inhibit chondrogenesis, while Wnt5a supports cartilage formation, but can impede Col2 expression and induce dedifferentiation. 39,42,43 These findings support the Wnt expression trends observed in our data, where both Wnt3a and Wnt5a were expressed in earlier stages following proliferation and FGF-2 supplementation but, following chondrogenic differentiation, Wnt3a and Wnt5a mRNAs and proteins were either significantly decreased or undetected. This expression is likely important in maintaining the ''stemness'' of the SDSCs, which may promote successful responses to chondrogenic media, as well as later expression of Col2, aggrecan, and greater GAG deposition.…”

Computational Systems Biology of Psoriasis: Are We Ready for the Age of Omics and Systems Biomarkers?

“…WNT5A stimulates the production of several inflammatory cytokines and chemokines, such as IL6, CXCL1, and CXCL8. WNT5A also binds to several members of the Frizzled receptor family, including FZD5 ( Jung, 2013), and is inhibited by WIF1 (Surmann-Schmitt et al, 2009). FZD5 was upregulated and WIF1 was downregulated in our analysis.…”