Stem Cells in Old Muscles: Fountain of Youth? New Study Reveals Promising Results
Can Mice Muscles Show Us How To Reverse The Aging Process?
A study, soon-to-be-published in the journal Nature, involving researchers from King's College London, Harvard University and Massachusetts General Hospital, reveals that stem cells in muscles - which are responsible for muscle repair -- may be able to regenerate - instead of die - as we age. Could this be a way to stay young forever?
"...People are not dying as early as they used to, but the body hasn't figured out how to maintain its muscle repair," Andrew Brack, of the Massachusetts General Hospital Center for Regenerative Medicine and corresponding study author, told FoxNews.com.
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Inside of our muscles, scientists know now that there are pools of stem cells, waiting to be activated when needed. Say you exercise and tear a muscle, and the muscle needs a repair job. These stem cells, when alerted, will jump into appropriate action: they divide into hundreds of new muscle fibers that repair the muscle, and also replenish the pool of dormant stem cells so that the muscle retains the ability to repair itself again and again. When necessary.
Trouble is, the number of dormant stem cells declines as we age. So there are less ready-in-waiting little soldiers to jump into action when the need arises. This could explain why as we age, muscles do tend to lose the ability to repair, bounce back and regenerate as quickly as they used to. (The old grey mare - she ain't what she used to be.)
Older muscles have been found to have higher levels of a certain protein called FGF2. FGF2 actually stimulates cell division. Also, FGF2 can activate regeneration when it is not needed...so higher levels may cause quicker depletion of the stem cell pool.
As reported by ScienceDaily, after the researchers made this discovery, they experimented with inhibiting FGF2 in old muscles (of elderly mice!) in order to prevent the stem cell pool from being kick-started into action when it was not needed. They injected a common FGF2 inhibitor drug, and successfully inhibited the decline in the number of stem cells in the mice muscles.
"We think of this as the first study where we've identified something that goes wrong in the aging muscle," Basson, senior lecturer at King's College London Dental Institute, told FoxNews.com.
"As your muscle gets old, you start making more of this FGF2 protein," said Basson. And when there's more of the protein mulling around in the muscle cell, the FGF2 starts waking up these stem cells and they start dividing. Trouble is, the stem cells have a limited number of times they can divide before they die or differentiate into other cells."
The scientists tried boosting a gene called SPRY2. (Great moniker, isn't it, for a muscle gene?) And so the study involved researchers giving a common drug containing SPRY2 to the mice, to suppress FGF2 levels in elderly mice.
And it worked. The drugs actually halted the decline of muscle stem cells in the mice. But - as is often the case in science (and life itself) ...there's a twist. Perhaps you could call it a side effect.
FGF2 protein is still necessary for activating stem cells when muscles do experience injury.
Because of this paradox and challenge to the idea of a magical fix-it, Brack says he imagines a future drug that will include SPRY2, but would be used only during periods of little physical effort - perhaps a time-released injection or pill.
For the future? Brack and Basson do project that their study results will lead to human therapies. However, they do not see this as a method to increase longevity, but rather, as a way to enhance living as we age.
"The purpose," explained Brack to Foxnews, "is not to live to 120, but to see how healthy and vital you can be. That's the future of regenerative medicine."
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