LOS ANGELES, June 16 (Xinhua) -- Researchers at the
University of California in Berkeley are a step closer to understanding how a
series of molecular switches can turn on or off the regenerative power of stem
cells that normally build new muscle tissue after ithas been damaged, the San
Francisco Chronicle reported on Monday.
The research, conducted on laboratory mice, is years
away from practical therapies for human beings. Nevertheless, this latest work
provides insight into how scientists are dissecting, step-by-step, the processes
that govern how stem cells work.
A goal of such research is to find ways to intervene
and control these molecular switches -- to improve healing and perhaps slow the
effects of aging.
The research was carried out by Irina Conboy and her
colleagues at the Department of Bioengineering. They are trying to solve one of
the mysteries of aging: why muscle cells readily repair themselves when we are
young, but are slower to do so as we grow older.
About 2 percent of cells in muscle tissue are
"satellite" cells. These tiny powerhouses are adult stem cells, which uniquely
can be coaxed into producing new muscle fibers with the right set of chemical
signals.
Conboy contends that the stem cells within older
tissue are no different from those found in young muscle -- the difference over
time appears to occur in the chemicals that switch them on or off. In effect,
she explained, the stem cells don't wear out, but the switches do.
So the key to repairing older muscle tissue is to
understand how these switches work, and how to restore their function as they
wear out. An important finding in the newly published research is that these
signals compete to turn these stem cells on or off. As muscle tissue ages, the
outcome of that competition tends to tip against renewal.
"We need to figure out how the on-and-off switches
become deregulated, then how to recalibrate them back to the young state,"
Conboy said. "Then the stem cells in the old tissue will start working as well
as in the young tissue. The goal for humans is to regenerate tissue as if you
were 25 years old."
Conboy's research was done with laboratory mice. Both
mice and men have similar systems of muscular repair using adult stem cells.
The regenerative capacity in the muscle of a
2-year-old mouse is similar to that of an 85-year-old human. So Conboy's lab
studied both young mice and 2-year-old mice to compare how the molecular
switches for stem cells perform in the old and young.
The mouse studies showed that the two competing
chemical signals strike a constant, shifting balance with each other. In younger
mice, there are higher levels of the on switch, and lower levels of the off
switch; in older mice, the balance is reversed. As a consequence, muscle tissue
is readily repaired in young mice, whereas it is a slower process among the
older rodents.
What remains unexplained is precisely what causes
this balance to change -- why these chemical switches wear out. That is a topic
likely to keep researchers busy in their labs for years to come.