The Wnt receptor Frizzled-9 (Fzd9) promotes bone formation, providing a potential new target for the treatment of osteoporosis, new research has shown.
The study appears online on March 14 in The Journal of Cell Biology (www.jcb.org).
Adult bones are maintained by a balance of bone-forming osteoblasts and bone-resorbing osteoclasts. Although Wnt signaling affects this balance in mice and humans, the Wnt receptors involved remain unknown. A team of researchers led by Thorsten Schinke found that the Wnt receptor Fzd9 was upregulated during osteoblast differentiation and that mice lacking Fzd9 had fragile bones due to low rates of bone formation.
Mice lacking one copy of Fzd9 also had low bone mass, suggesting that insufficient Fzd9 may cause the reduced bone density seen in Williams-Beuren syndrome patients, who have a hemizygous deletion of the chromosomal region that includes the FZD9 gene. Schinke now wants to investigate whether boosting Fzd9 expression has the opposite effect to Fzd9 depletion and can stimulate bone formation. If so, Fzd9 would be an attractive drug target for treating a variety of bone-loss disorders.