Physical activity that puts mechanical stress on bones stimulates new bone growth. Osteocytes, which account for 90-95% of all bone cells, help detect mechanical stress on bone. They then regulate impaired bone breakdown by cells called osteoclasts and the formation of new bone by cells called osteoblasts.
First author Dezhi Zhao, a doctoral student at the University of Texas Health Science Center at San, explains: “Previous research has shown that mechanical stress on bone increases the number of upper channels surface of bone cells, called channel binding (Cx) 43. Antonio, Texas, USA. “In this study, we wanted to examine the role of these channels in the response to mechanical stress to bone.”
To do this, Zhao and his team studied two types of mouse models. In it, connections between osteocytes, called gap junctions, are impaired but Cx43 platelet channels are enhanced. On the other hand, both the cleft junction and the Cx43 molecular channel are attenuated. The team then examined what happened to the bones of these mice, as well as typical mice, when exposed to mechanical stress.
They found that a chemical called prostaglandin (PGE2) was made in both typical and gap-deficient mice in response to mechanical stress, and their bones became stronger. On the other hand, this response is lacking in mice with impaired blood molecule Cx43.
To confirm that Cx43 platelet channels are essential for bone strengthening, the team then gave typical mice an antibody that blocks the activity of the Cx43 platelet channel. They found that this also prevented the animals from releasing PGE2 and reduced bone strength in response to mechanical stress. But treating the same mice with PGE2 restored the bone-strengthening effects of mechanical stress.
Current treatments for osteoporosis typically target osteoclasts that help break down weakened bone and work by reducing bone turnover. This can inadvertently lead to more brittle bones over time and is associated with some rare but serious side effects. The present study suggests that targeting Cx43 blood channels on osteocytes may be an alternative treatment option that utilizes the body’s own response to mechanical stress.
Senior author Jean Jiang, Professor and President of Zachry University, Department of Biochemistry and Structural Biology, UT Center for Health Sciences in San Antonio. “Further studies are needed to verify these findings and explore the potential of drugs that target these channels. If they are to one day prove to be safe and effective, then what are these methods?” Such treatment may be particularly helpful for older patients who are poorly responsive to bone strengthening to the effects of motion.”
Source: Eurekalert
