Scientists have identified a protein that blocks the activity of bone-forming cells (osteoblasts) by preventing them from maturing during their migration to sites of bone formation, a new study finds. .
In a paper published today (Friday 11 October 2024) in Communications Biology, a research team led by Dr Amy Naylor and Professor Roy Bicknell, and including Dr Georgiana Neag from the University of Birmingham, said: Discovered the protein CLEC14A. It blocks the function of bone-forming cells called osteoblasts on blood vessel cells called bone endothelial cells.
The job of endothelial cells during bone development is to transport immature osteoblasts to the site where new bone is needed. However, when the protein CLEC14A is also present on the outside of endothelial cells, it prevents osteoblasts from maturing to the point where they can form bone tissue.
In this study, osteoblasts were harvested from transgenic mice that were bred to produce CLEC14A or not. When osteoblasts were then used in vitro in an induction solution, cells from mice without the protein reached maturity after 4 days, whereas cells in the presence of CLEC14A reached maturity after 8 days. It turns out. Additionally, samples without CLEC14A showed a significant increase in mineralized bone tissue at day 18 of the study.
Dr Amy Naylor, Associate Professor in the Department of Infection, Inflammation and Immunology at the University of Birmingham, said:
“Over the past decade, a specific type of vascular cell has been identified within bone. This blood vessel, called ‘H-type,’ is responsible for guiding bone-forming osteoblasts to where bone growth is needed. is in charge of A protein called CLEC14A is known to exist on the surface of type H blood vessel cells.
In our experiments, the presence of the CLEC14A protein reduced the amount of bone produced by osteoblasts that were co-opted by endothelial cells. Conversely, when protein is removed, more bone is produced. ”
Dr Amy Naylor, Associate Professor, Department of Infection, Inflammation and Immunology, University of Birmingham
“Further understanding of how vascular cells control bone-forming osteoblasts in normal, healthy conditions will help patients with insufficient bone formation, for example in patients with non-healing fractures, osteoporosis, or chronic inflammatory diseases. It provides an avenue to develop treatments for patients.”
Lucy Donaldson, Director of Research and Health Intelligence at Versus Arthritis, said:
“We know that poor bone formation is an important factor in bone damage in osteoporosis and autoimmune inflammatory arthritis. It affects people’s lives in many ways, including time, family, friends, and their health.
We are proud to have funded Dr. Naylor’s research that has advanced our understanding of bone formation and remodeling. We hope that these discoveries will eventually lead to new treatments for people with musculoskeletal diseases.
While these discoveries are promising, we will not rest until all people with arthritis have access to treatments and interventions that allow them to live the life they choose. ”
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Reference magazines:
Neag, G., Lewis, J., Turner, J.D., Manning, J.E., Dean, I., Finlay, M., Phoolgasundarampilai, G., Woods, J., Sahu, M.A., Khan, K.A. Begum, J., McGettrick, H. M., Bellantuono, I., Heath, V., Jones, SW., Buckley, CD., Bicknell, R., and Naylor, A. J. (2024). The H-type endothelial cell protein Clec14a regulates osteoblast activity during cancellous bone formation and patterning. Communication Biology, 7(1). https://doi.org/10.1038/s42003-024-06971-3
