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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Glucocorticoid suppresses the canonical Wnt signal in cultured human osteoblasts.

To explore the mechanism of glucocorticoid-induced osteoporosis, we investigated the effect of glucocorticoid on canonical Wnt signaling that emerged as a novel key pathway for promoting bone formation. Wnt3a increased the T-cell factor (Tcf)/lymphoid enhancer factor (Lef)-dependent transcriptional activity in primary cultured human osteoblasts. Dexamethasone suppressed this transcriptional activity in a dose-dependent manner, while 1,25-dihydroxyvitamin D3 increased this transcriptional activity. LiCl, an inhibitor of glycogen synthase kinase-3beta, also enhanced the Tcf/Lef-dependent transcriptional activity, which was, however, not inhibited by dexamethasone. The addition of anti-dickkopf-1 antibody partially restored the transcriptional activity suppressed by dexamethasone. Dexamethasone decreased the cytosolic amount of beta-catenin accumulated by Wnt3a and also inhibited the nuclear translocation of beta-catenin induced by Wnt3a. These data suggest that glucocorticoid suppresses the canonical Wnt signal in cultured human osteoblasts, partially through the enhancement of the dickkopf-1 production.[1]

References

  1. Glucocorticoid suppresses the canonical Wnt signal in cultured human osteoblasts. Ohnaka, K., Tanabe, M., Kawate, H., Nawata, H., Takayanagi, R. Biochem. Biophys. Res. Commun. (2005) [Pubmed]
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