Young blood revives aging muscles

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Young blood revives aging muscles

Posted By: News-Medical in Medical Research News

Published: Wednesday, 16-Feb-2005

Any older person can attest that aging muscles don't heal like

young ones. But it turns out that's not the muscle's fault. A study in the Feb.

17 issue of Nature shows that it's old blood that keeps the muscles down.

The study, led by Rando, MD, PhD, associate professor

of neurology and neurological sciences at the Stanford University School of

Medicine, built on previous work showing that old muscles have the capacity to

repair themselves but fail to do so. Rando and his group studied specialized

cells called satellite cells, the muscle stem cells, that dot muscle tissue.

These normally lie dormant but come to the rescue in response to damaged

muscle-at least they do in young mice and humans.

In older mice the satellite cells hold the same position, but

are deaf to the muscle's cry for help. In the Nature study, Rando and his group

first attached old mice to their younger lab-mates in a way that caused the two

mice to share a blood supply. They then induced muscle damage only in the older

mice. Bathed in the presence of younger blood, the old muscles healed normally.

In contrast, when old mice were connected to other old mice they healed slowly.

In similar work, the group examined the livers of older mice

connected to younger lab-mates. The cells that help liver tissue regenerate are

less active in older animals, but again the cells responded more robustly when

the livers in older mice were bathed in the younger blood. Clearly, something in

the youthful blood revived the regenerative cells in muscle and liver.

" We need to consider the possibility that the niche in which

stem cells sit is as important in terms of stem cell aging as the cells

themselves, " said Rando, who is also an investigator at the Veterans Affairs

Palo Alto Health Care System. It could be the chemical soup surrounding the

cells, not the cells themselves, that's at fault in aging.

One clue to what might be going on also comes from previous

work. Rando had found that satellite cells in younger muscles begin producing a

protein dubbed Delta in response to muscle damage. Older muscles maintained the

same pre-injury levels of Delta even after muscle damage. However, in the

current study he found that satellite cells in elderly mice joined to younger

partners ramped up Delta production to youthful levels after an injury.

The group confirmed their results by putting satellite cells

from old and young mice in a lab dish with either old or young blood serum. Old

satellite cells in old serum and young satellite cells in young serum both

behaved as expected. But when old satellite cells were bathed in young serum

they cranked up their production of Delta and began dividing. Likewise, young

satellite cells decreased the amount of Delta they produced when in a dish with

older serum and divided less frequently.

Rando said that it may be a general phenomenon that a person's

inability to repair tissues with age-whether it's muscle, liver, skin or

brain-is a matter of the regenerative cell's environment rather than the cells

themselves.

Rando said that finding the youth-promoting factors in the

blood is no small task. " It's as big a fishing expedition as you can possibly

imagine, " he said. With thousands of proteins, lipids, sugars and other small

molecules in the blood serum, deciding where to look first would be tantamount

to a roll of the dice. What's more, there's no evidence that the same blood

component is responsible for reviving the different types of cells.

" Another approach is to pick factors that are good candidates

and see if any of them or some combination recapitulate the effect of the

younger blood, " Rando said. His group is now looking for likely targets. He said

that for some degenerative diseases such as Alzheimer's or muscular dystrophy,

such blood-borne factors may be able to reactivate the regenerative cell's

ability to repair tissue that has been damaged.

http://med-www.stanford.edu

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