'Frizzled' protein levels may affect osteoporosis development
New research has determined that a specific protein signals bone-forming cells to create bone minerals, a finding which may lead to new treatments for osteoporosis.
The study, which appears in the Journal of Cell Biology
, found that disruption of the Wnt receptor Frizzled-9 (FZD9) appears to inhibit bone growth regulated by osteoblasts.
A team of German geneticists and bone health experts came to this conclusion after examining the consequences of the disruption in laboratory mice. They theorized that this protein may be an important link in the protein-based messaging system that regulates bone growth.
Osteoblasts are specialized cells that create bone minerals. Partner cells, called osteoclasts, break down that bone tissue. In a healthy individual, these two processes are essentially in equilibrium. In a person with osteoporosis, however, osteoclasts outpace their counterparts, leading to low bone mineral density.
The new study's authors, who hail from the University Medical Center Hamburg-Eppendorf, noted the role of FZD9 in osteoblast stimulation after examining the bone density of mice that lack the protein.
They found that these rodents, unlike their FZD9-positive peers, had weak bones. On closer examination, researchers found that FZD9-negative mice had a normal number of osteoblasts, but that these cells failed to create a hard, mineralized shell around themselves.
The team also attempted to follow the chain reaction caused by the absence of FZD9. They noted that several subsequent proteins did not get expressed, including a molecule called ISG15. Though scientists are unsure what ISG15's function is within the body, they found that reintroducing it into the bodies of FZD9-negative mice increased bone production.
In conclusion, the authors suggested that FZD9 would make an effective target for potential drugs designed to treat osteoporosis.
More than 41 million Americans will have either low bone mass or osteoporosis by the year 2020, according to the National Osteoporosis Foundation.