Scientists have discovered a protein that inhibits the function of bone-forming cells, known as osteoblasts, by preventing their maturation on their way to bone formation sites, according to a recent study.
Scientists have discovered a protein that inhibits the function of bone-forming cells, known as osteoblasts, by preventing their maturation on their way to bone formation sites, according to a recent study.
A research team led by Dr. Amy Naylor and Professor Roy Bicknell, alongside Dr. Georgiana Neag from the University of Birmingham, published a paper today in Communications Biology that highlights this finding. The protein CLEC14A, found on endothelial cells (the cells lining blood vessels) in bone, disrupts the activity of osteoblasts.
Endothelial cells play a crucial role in bone development by transporting immature osteoblasts to the locations where new bone formation is required. However, when CLEC14A is present on the surface of these endothelial cells, it prevents the osteoblasts from maturing enough to create bone tissue.
For this study, the researchers used osteoblast cells from transgenic mice engineered to produce CLEC14A and those that do not. The osteoblasts were studied in an induction solution in the lab, and the results showed that the cells from mice without CLEC14A matured after just four days, while those with the protein took eight days longer. Additionally, the samples without CLEC14A showed a notable increase in mineralized bone tissue after 18 days.
Dr. Amy Naylor, an Associate Professor in the School of Infection, Inflammation and Immunology at the University of Birmingham, elaborated:
“In the past ten years, a specific type of blood vessel cell, known as ‘type-H,’ has been identified within bones. This type-H blood vessel cell facilitates the transport of bone-forming osteoblasts to areas needing new bone growth. We have now found that CLEC14A is present on the surface of these type-H blood vessel cells.
“Our experiments revealed that the presence of CLEC14A causes osteoblasts sharing transport with endothelial cells to produce less bone. In contrast, when this protein is absent, these cells generate more bone.”
“This deeper insight into how blood vessel cells regulate osteoblasts under normal conditions opens up possibilities for developing treatments for patients experiencing insufficient bone formation, such as those with non-healing fractures, osteoporosis, or chronic inflammatory diseases.”
Lucy Donaldson, Director for Research & Health Intelligence at Versus Arthritis, stated:
“Poor bone formation significantly contributes to bone damage in conditions like osteoporosis and autoimmune inflammatory arthritis. This can cause disability, pain, and fatigue, severely affecting individuals’ daily lives, including their work, social interactions, and overall well-being.
We are pleased to have supported Dr. Naylor’s research, which has advanced our understanding of bone formation and remodeling. We hope these findings will eventually lead to innovative treatment methods for those with musculoskeletal conditions.
While these results are encouraging, we are committed to ensuring that everyone with arthritis has access to effective treatments and interventions that enable them to lead fulfilling lives.”
