Why do vampires from Dracula to Angel seem to crave the blood of the young and beautiful? The undead may be onto something.
The Young blood, it seems, has special healing properties that have been lost in older blood.
“The traditional concept is that as you get older, your bone cells kind of wear out so they can’t heal as well, and we thought we’d find that during this study as well,” explains study co-author Benjamin Alman, of the Hospital for Sick Children. “But it turns out that it’s not the bone cells, it’s the blood cells. As you get older, the blood cells change the way they behave when you have an injury, and as a result, the cells that heal bone aren’t able to work as efficiently.”
When a bone is fractured, significant bleeding occurs at the site. Inflammatory blood cells help spur the process by which new bone cells heal the break over time. Alman and colleagues found that the blood cells of older mice don’t drive this healing the way younger blood cells do, but they also wanted to see how those older bones would heal when exposed to young blood.
The researchers paired lab mice, one old and one young, and subjected them to bone fractures, but that wasn’t all they had in common. The living animals’ circulatory systems were also joined together by a 150-year-old surgical technique known as parabiosis. Scientists removed a layer of skin from each mouse and stitched the exposed surfaces together. As the animals healed their capillaries joined, enabling their two hearts to pump the same blood throughout the two bodies as a single system. Parabiosis, which has been gaining new popularity in aging research, allowed Alman and colleagues to see what impacts the circulating factors of the younger mouse’s blood had when introduced into the body of an older mouse.
The experiment, published this week in Nature Communications, suggests that young blood cells secrete some as-yet-unknown molecule, likely a protein or possibly some other chemical, that speeds up the healing of fractured bone. The molecule apparently does so by regulating levels of beta-catenin in bone cells known as osteoblasts. Keeping beta-catenin at the proper levels appears crucial for the formation of new high-density bone.
This ability is greatly diminished in older animals’ blood because it no longer secretes the molecule, whose exact chemical nature remains a mystery at this point. “My guess is that there are a number of proteins involved that are made differently as we get older and that they are responsible for the difficulty in healing bone,” Alman says.
The findings could prove good news for aging humans, but healing our bones won’t require the type of transfusions used in the experiment—nor will it borrow the synthesized “True Blood” variety that may soon enter clinical trials. Sharing human blood in this manner raises a number of red flags ranging from practicality to possible medical complications.
Instead, the critical next step is identifying the exact chemical nature of the molecule produced by young blood cells that older cells can no longer secrete. Pinpointing it could drive the development of future drugs that would help enable older bone cells to work as they did in youth, by either spurring older blood to function more as younger blood does or by simply delivering the proteins that the blood once did, enabling bone cells to do their healing work.
“It’s not the cells responsible for making new bone that has changed,” Alman says. “[Bone cells] still have that ability to act like they are young again.”
“If they could never behave like young cells again, and they were too worn out to produce bone the way they should, it would be really hard to change that,” he adds. “But these results show that this is a solvable problem. Now it’s a matter of figuring out how best to make it work.”