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Throughout our lives, our bones undergo constant remodeling. Cells called osteoclasts break down old bone and cells called osteoblasts lay down new. Normally, the two cell types work in balance but if the rate of breakdown outpaces new bone formation the skeleton can become weak. This weakness leads to a condition called osteoporosis, in which people suffer from fragile bones. Osteoporosis is hard to reverse, in part because our ability to encourage new bone to form is limited.
In 2016, researchers discovered a protein called osteolectin, which promotes new bone formation during adulthood by helping skeletal stem cells transform into bone cells. But so far, it has been unclear how osteolectin achieves this. To investigate this further, Shen et al. – including some researchers involved in the 2016 study – marked osteolectin with a molecular tag and tested what it bound on the surface of mouse and human bone marrow cells.
The experiments revealed that osteolectin binds to a specific receptor protein called α11 integrin, which can only be found on skeletal stem cells and the osteoblasts they give rise to. Once osteolectin binds to the receptor, it activates a signaling pathway that induces the stem cells to develop into osteoblasts. Mice that lacked either osteolectin or α11 integrin produced less bone and lost bone tissue faster as adults.
Osteolectin could potentially be useful in the treatment of osteoporosis or broken bones. Since only skeletal stem cells and osteoblasts cells produce α11 integrin, osteolectin would specifically target these cells without affecting cells that do not form bones. A next step will be to assess how well osteolectin compares to existing treatments for fragile bones.
