WASHINGTON, July 27 (Xinhua) -- Too little of a protein called neogenin results in a smaller skeleton during development and sets the stage for a more fragile bone framework lifelong, researchers at Medical College of Georgia (MCG) reported.
A developing mouse with neogenin deficits has poorly defined digits and is generally smaller, including having small growth plates, an indicator of future development, said Dr. Wen-Cheng Xiong, developmental neurobiologist in the MCG Schools of Medicine and Graduate Studies and corresponding author of the study published Tuesday in Developmental Cell. Dr. Zheng Zhou, MCG assistant research scientist, is first author.
Their findings provide new insight into skeletal development as they point toward a potential new direction for treating osteoarthritis, a common, painful and debilitating condition where cartilage between bones is lost, Xiong said.
Neogenin doesn't make bone; rather, it forms a protein complex essential to turning on cartilage-producing genes, the researchers found. "Each cell type has a master gene. Neogenin is not that, it 's more of a modulator," Xiong said.
That's why, if it's mutated, like in the mouse, cartilage and bone formation is disrupted -- not halted. It's also why neogenin could be a good therapeutic target for turning the tide on cartilage or bone loss that occurs in osteoarthritis, Xiong said.
