Research illuminates how stem cells may work
Sabin Russell, Chronicle Medical Writer
Monday, June 16, 2008
(06-15) 11:21 PDT -- UC Berkeley scientists 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 it has been damaged.
The research, conducted on laboratory mice, is years away from
practical therapies for human beings. Nevertheless, this latest work,
published online Sunday by the journal Nature, 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.
"How can you fix a car if you don't know how the engine looks?" said
Rik Derynck, co-director of the Institute for Regeneration Medicine
at UCSF, who was not involved in the Berkeley research but is
conducting similar studies in his lab. "We are all trying to find out
what's really happening inside these stem cells."
Although Derynck is skeptical that the work will have much impact in
slowing the aging process, he believes the approach could lead,
within five to 10 years, to novel therapies against degenerative
diseases such as muscular dystrophy.
The UC Berkeley 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.
In earlier work, Conboy's team identified a protein called Notch that
acts as an on switch. It stimulates adult stem cells to begin
morphing into new muscle fiber cells and multiplying. The body uses
this sequence all the time to repair torn muscles or replace worn-out
tissues.
But her work also found that the presence or absence of Notch alone
did not fully control the repair process. The latest study identified
another protein - with the unfortunate moniker pSmad3 - as an off
switch for adult stem cells.
Even if the body were producing Notch to stimulate repair, the stem
cells might remain quiet if the body were also churning out more of
the off switch pSmad3.
Why would the body want to turn off a repair process? One reason may
be that cell growth stimulation can promote cancers. Another reason
may be to conserve a limited lifetime supply of adult stem cells, so
they are activated only when needed.
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.
"When the death of tissue is faster than repair, many, many diseases
begin to appear," Conboy said.
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.
E-mail Sabin Russell at srussell@sfchronicl
This article appeared on page B - 1 of the San Francisco Chronicle
http://www.sfgate.
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StemCells subscribers may also be interested in these sites:
Children's Neurobiological Solutions
http://www.CNSfoundation.org/
Cord Blood Registry
http://www.CordBlood.com/at.cgi?a=150123
The CNS Healing Group
http://groups.yahoo.com/group/CNS_Healing
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