Xenbase Image ID: 155601

Figure 5. WNT16 is a weak activator of the β-catenin-dependent pathway but also limits its activation by other more potent canonical WNTs. WNT16 caused a weak upregulation of the canonical WNT reporter gene Axin2 compared with WNT3a, in human articular chondrocytes (HAC) (N=3 patients, 4 replicates each) (A). Lubricin expression caused by WNT16 stimulation (ng/mL) in HAC (B), and mouse superficial zone cell (SZC) (C), was higher than that caused by WNT3a stimulation. Lubricin expression decreased in the presence of canonical inhibitor DKK1 (100 ng/mL) in mouse SZC (N=4) (C). All at 24 h. Following destabilisation of the medial meniscus (DMM) surgery, wnt16−/− mice had a higher expression of Axin2 mRNA in their joints (D). WNT16 reduced the capacity of WNT3a to activate the SUPER8XTOPFlash reporter assay in HEK293 cells treated with WNT3a, alone and in combination with WNT16 (ng/mL) (N=4) (E and F). wnt16 inhibited axis duplication caused by wnt8 in Xenopus laevis (G and H). Embryos were injected ventrally with 0.02 ng/µL wnt16 or 0.002 ng/µL wnt8 at the four-cell stage and left for 2 days to develop (n=36–47). Image published in: Nalesso G et al. (2017) Published by the BMJ Publishing Group Limited. This image is reproduced with permission of the journal and the copyright holder. This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial license Larger Image Printer Friendly View

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