Protein That Controls Hair Growth Also Keeps Stem Cells Slumbering
ScienceDaily (Jan. 25, 2008) — Like fine china and crystal, which
tend to be used sparingly, stem cells divide infrequently. It was
thought they did so to protect themselves from unnecessary wear and
tear. But now new research from Rockefeller University has unveiled
the protein that puts the brakes on stem cell division and shows that
stem cells may not need such guarded protection to maintain their
potency.
This research, to be published in the January 25 issue of Cell,
raises questions about what stem cells need in order to maintain
their ability to regenerate tissue. It may also be key in developing
new treatments for thinning hair.
The impetus for the work began five years ago when Elaine Fuchs, head
of the Laboratory of Mammalian Cell Biology and Development, and
several researchers in her lab discovered that the protein NFATc1 was
one of only a few that are highly expressed within the stem cell
compartment of the hair follicle. Clinical research, meanwhile,
showed that a particular immunosuppressant that inhibits NFATc1, a
drug called cyclosporine A, has a rather unsightly side effect:
excessive hair growth.
Fuchs and Valerie Horsley, a postdoc in her lab, realized that there
was a connection between the drug's side effect and the abundance of
NFATc1 within the hair follicle's stem cell compartment -- the bulge.
The mice they treated with the drug grew fur at a much faster rate
than mice they did not treat. The researchers then showed that this
excessive hair growth was due to increased stem cell activity within
the bulge, a process that cranked up the production of hair.
Specifically, the hair cycle shifted gears from its resting phase,
when stem cells slumber, to its growth phase, when stem cells
proliferate.
To maintain their multipotent properties, though, it appears that
these stem cells hardly needed much "rest" at all. These findings
came as a surprise to the researchers, who, like their colleagues,
had believed that stem cells proliferating infrequently protected
them from depletion or mutations that would lead to hair loss. "It
seems like the resting phase isn't as necessary as was once thought,"
says Horsley. "Even though these stem cells are highly proliferative,
they still maintain their stem cell character."
Using genetically engineered mice bred by colleagues at Harvard
Medical School, Horsley and Fuchs then further explored what happens
when skin stem cells lack NFATc1. They found that these mice looked
exactly like the hairy mice that were treated with cyclosporine A:
The loss of NFATc1 didn't stop the hair cycle, but rather shortened
the resting phase and prompted precocious entry to the growth state.
In probing the underlying mechanisms mediating this process, Horsley
and Fuchs discovered that NFATc1, a transcription factor, blocks the
expression of a gene that provides the cell cycle with "go ahead"
signals at certain checkpoints. By blocking these signals, NFATc1
prevents the stem cells from dividing, preventing unnecessary wear
and tear. These same cells, if treated with cyclosporine A, show a
rapid loss of the transcription factor, an effect that turns the
light green at these checkpoints.
For those with thinning hair, this research may hold promise. As
people age, the resting phase of the hair cycle gets longer and
longer such that the stem cells proliferate less frequently and hair
does not grow at the rate it once did. "If we could use a local and
more specific inhibitor of NFATc1 than cyclosporine A to stimulate
these stem cells, which are just sitting there during an extended
resting phase, we might be able to promote new hair growth," says
Fuchs, who is Rebecca C. Lancefield Professor at Rockefeller and an
investigator at the Howard Hughes Medical Institute. "In a sense, by
blocking NFATc1 activity in our older mice, their hair follicles were
brought back to what appeared to be a more youthful state."
So far, these proliferating stem cells lacking NFATc1 have not led to
increased tumor formation, which is often a dangerous byproduct of
triggering stem cells into action. "This is the first case where we
have been able to activate the hair cycle without accompanying signs
of tumorigenesis,
process of follicle stem cells without promoting tumorigenesis, then
this would be a big move in the right direction."
This research was supported in part by the National Institutes of
Health, American Society for Clinical Investigation and the Damon
Runyon Cancer Research Foundation. Fuchs is a faculty member in
Rockefeller'
supported by the NIH's Clinical and Translational Science Award
(CTSA) program.
Adapted from materials provided by Rockefeller University, via
EurekAlert!, a service of AAAS.
Need to cite this story in your essay, paper, or report? Use one of
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MLA Rockefeller University (2008, January 25). Protein That Controls
Hair Growth Also Keeps Stem Cells Slumbering. ScienceDaily. Retrieved
January 24, 2008, from http://www.scienced
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