Researchers at the University of Birmingham in the UK have identified a protein that inhibits the development of osteoblasts. The study used multiple approaches to determine the impact of this protein on osteoblast development and how its absence changes bone formation.
In this article we'll examine the study, what it reveals about the bone development process, and how it may influence the future of bone health interventions, including the potential for new drug development.
Newly Identified Protein Impacts Osteoblast Development
A study published in October 2024 in the journal Communications Biology identified a protein found on a specific type of endothelial cell known as type-H endothelial cells.
Endothelial cells line blood vessels. In the past decade, researchers discovered a unique type of blood vessel within bone tissue, called Type-H blood vessels. Type-H endothelial cells aid the bone remodeling process by transporting immature osteoblasts to sites in need of new bone tissue. Osteoblasts are the cells responsible for creating new bone material.
Researchers identified a protein that can be found on Type-H endothelial cells called CLEC14A. Their study concluded that protein CLEC14A delays the development of immature osteoblasts, delaying or preventing them from depositing new bone material.1
Synopsis
Type-H endothelial cells transport immature osteoblasts to sites of bone deposition. New research has identified a protein called CLE14A which delays the development of those immature osteoblasts if it is also present on the endothelial cells.
Tracking The Impact Of An Osteoclast-Suppressing Protein
The study's authors confirmed the effects of the CLEC14A protein on osteoblasts through various methods.
The researchers observed mice bred either to produce CLEC14A normally or not to produce the protein. These genetic knock-out mice allowed the researchers to measure the impacts of the protein.
The researchers observed and recorded differences in bone formation between the two groups of mice. Mice lacking the CLEC14A protein exhibited “increased long-bone length and bone density indicative of accelerated skeletal development, and enhanced osteoblast maturation.”1
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The researchers also examined the protein by isolating immature osteoblasts from both groups of mice and observing their development in the laboratory. They found that the osteoblasts taken from mice without the CLEC14A protein matured in four days. The osteoblasts from mice with the protein took 8 days to develop.
The researchers identified CLEC14A as a vital component of cellular crosstalk acting as a signal to slow down osteoblast maturation. The study concluded that their finding “underscores the importance of type-H capillary control of osteoblast activity in bone formation and identifies a novel mechanism that mediates this vital cellular crosstalk.”
Synopsis
The researchers conducted their study with two groups of mice, one normal, and one without the ability to produce protein CLEC14A. They examined the mice's bones and found mice without CLEC14A had denser bones with more mature osteoblasts. They also removed immature osteoblasts from both groups of mice and observed that exposure to CLEC14A delayed maturation.
The Relevance Of An Osteoblast-Regulating Protein
The CLEC14A protein is part of a complex system regulating osteoblast development and bone remodeling. These findings offer new insights into how our bodies function and highlight the importance of type-H blood vessels and endothelial cells. This blood vessel type was only identified in the last decade. Research on its function is still uncovering significant new discoveries.
This study shows that CLEC14A can prevent and delay osteoblast maturation and bone deposition, at least in mice. Further research is needed to determine if these processes occur in human bone.
This raises new questions such as: are there behaviors that encourage the overproduction of CLEC14A, hindering bone formation? Could certain behaviors reduce CLEC14A levels, enabling more osteoblasts to mature fully and effectively build new bone? These would be useful discoveries for improving bone health without the development of new drugs.
However, the scientific research process is so dominated by drug manufacturers that even this preliminary discovery is oriented toward drug development..
This passage from the study makes the researcher's intentions clear:
“The role of type-H EC (endothelial cells) in fracture healing and recent interest in harnessing them to support osteogenesis in osteoporosis is evidence of the potential of this cell type as a therapeutic target. To realise this potential, identification of druggable targets that control the interaction of type-H EC with osteoblasts is crucial. Here we identify Clec14a as a key endothelial cell-specific target protein, whose inactivation increases bone formation. Identification of entities that can modulate the activity of this protein will facilitate the dissection of the signaling pathways through which Clec14a exhibits its effects and may hold potential as novel bone anabolic therapeutics.”1
Unfortunately, this disappointing conclusion is typical of bone health research. However, Savers now know that new discoveries could lead to yet one more drug in development. The unintended side effects of this potential drug will be discovered later– possibly not until after it has been approved by the FDA.
The Save Institute will continue to monitor developments to keep Savers up-to-date and aware of any useful information that emerges from this line of research.
Synopsis
If CLEC14A has the same effect in humans as in mice, then it may be part of the bone remodeling process that can be modulated through behavioral changes. However, the researchers lean towards Big Pharma to develop drugs that would target CLEC14A. At the Save Institute, we will continue to monitor this research for new developments.
What This Means To You
Blood vessels in our bones contain endothelial cells that transport immature osteoblasts to sites in need of new bone material. This study identified a protein that inhibits the maturation of osteoblasts.
How this information will be applied and what remains to be discovered about how this protein functions in humans, as opposed to in mice, is yet to be seen. Staying on the cutting edge of research on bone health is imperative to stay ahead of Big Pharma's plans and to use discoveries to choose the best bone-healthy behaviors.
Behavioral shifts — changes in diet, physical activity, and lifestyle choices — constitute the all-natural strategies employed by the Osteoporosis Reversal Program. The program is based on decades of scientific study into how our bodies work and how our behaviors can radically improve our health and strengthen our bones.
Keep learning and keep taking sustainable steps toward an active and independent future.
Thank you for this deep digging giving insight in bone physiology. Fascinating!
You are right about pharmacology bias and narrow view.
In another health topic, it was most astounding to read about the use of thalidomide to alleviate the occurence of aphthous ulcers…
It would be simple enough to measure the amount of this new protein in people with various state of bone health.
One aspect of osteoporosis may lie in the fact of having poor bone density and strength to begin with as young adult due to some health issues when growing up. In late adolescence I grew up very quickly and suspect that my bone strength was poor to begin with. So my fracture at 55 years of age may be due to that rather than a steep decline in bone strength in the years before my fracture.
Yet, with hour program one cannot do wrong. Thanks again a. Million!
Thanks for sharing your story and for your kind words, Luc! And you’re very welcome 🙂