Why Does Hair Turn Gray? It Really is Due to Stress but You Cant
Blame the Spouse or Kids
Supports the "stem cell aging hypothesis," that DNA
damage to long-lived stem cells can be major cause for the symptoms that
come with age
June 11, 2009 Maybe you were right when you
blamed your spouse or children for your gray hair. Those pesky graying
hairs that tend to crop up with age really are signs of stress
genotoxic stress that is. A new report in the June 12 issue of Cell
says anything that can limit this stress might stop the graying from
happening.
The study discovered that the kind of genotoxic
stress that does damage to DNA depletes the melanocyte stem cells (MSCs)
within hair follicles that are responsible for making those
pigment-producing cells.
Rather than dying off, when the going gets tough,
those precious stem cells differentiate, forming fully mature
melanocytes themselves.
"The DNA in cells is under constant attack by
exogenously- and endogenously-arising DNA-damaging agents such as
mutagenic chemicals, ultraviolet light and ionizing radiation," said Emi
Nishimura of Tokyo Medical and Dental University.
"It is estimated that a single cell in mammals can
encounter approximately 100,000 DNA damaging events per day."
Consequently, she explained, cells have elaborate
ways to repair damaged DNA and prevent the lesions from being passed on
to their daughter cells.
"Once stem cells are damaged irreversibly, the
damaged stem cells need to be eliminated to maintain the quality of the
stem cell pools," Nishimura continued.
"We found that excessive genotoxic stress triggers
differentiation of melanocyte stem cells." She says that differentiation
might be a more sophisticated way to get rid of those cells than
stimulating their death.
Nishimura's group earlier traced the loss of hair
color to the gradual dying off of the stem cells that maintain a
continuous supply of new melanocytes, giving hair its youthful color.
Those specialized stem cells are not only lost, they also turn into
fully committed pigment cells and in the wrong place.
Now, they show in mice that irreparable DNA damage,
as caused by ionizing radiation, is responsible. They further found that
the "caretaker gene" known as ATM (for ataxia telangiectasia mutated)
serves as a so-called stemness checkpoint, protecting against MSCs
differentiation.
That's why people with Ataxia-telangiectasia, an
aging syndrome caused by a mutation in the ATM gene, go gray
prematurely.
The findings lend support to the notion that genome
instability is a significant factor underlying aging in general, the
researchers said.
They also support the "stem cell aging hypothesis,"
which proposes that DNA damage to long-lived stem cells can be a major
cause for the symptoms that come with age.
In addition to the aging-associated stem cell
depletion typically seen in melanocyte stem cells, qualitative and
quantitative changes to other body stem cells have been reported in
blood stem cells, cardiac muscle, and skeletal muscle, the researchers
said.
Stresses on stem cell pools and genome maintenance
failures have also been implicated in the decline of tissue renewal
capacity and the accelerated appearance of aging-related
characteristics.
"In this study, we discovered that hair graying,
the most obvious aging phenotype, can be caused by the genomic damage
response through stem cell differentiation, which suggests that
physiological hair graying can be triggered by the accumulation of
unavoidable DNA damage and DNA-damage response associated with aging
through MSC differentiation," they wrote.
Background Information:
The researchers include Ken Inomata,
Kanazawa University, Takaramachi, Kanazawa, Ishikawa, Japan, KOSÉ
Corporation, Tokyo, Japan, Hokkaido University Graduate School of
Medicine; Takahiro Aoto, Kanazawa University, Takaramachi, Kanazawa,
Ishikawa, Japan, Tokyo Medical and Dental University, Tokyo, Japan;
Nguyen Thanh Binh, Kanazawa University, Takaramachi, Kanazawa, Ishikawa,
Japan; Natsuko Okamoto, Kanazawa University, Takaramachi, Kanazawa,
Ishikawa, Japan, Kyoto University Graduate School of Medicine, Kyoto,
Japan; Shintaro Tanimura, Kanazawa University, Takaramachi, Kanazawa,
Ishikawa, Japan, Hokkaido University Graduate School of Medicine;
Tomohiko Wakayama, Kanazawa University, Ishikawa, Japan; Shoichi Iseki,
Kanazawa University, Ishikawa, Japan; Eiji Hara, The Cancer Institute,
Japanese Foundation for Cancer Research, Tokyo, Japan; Takuji Masunaga,
KOSÉ Corporation, Tokyo, Japan; Hiroshi Shimizu, Hokkaido University
Graduate School of Medicine; and Emi K. Nishimura, Kanazawa University,
Takaramachi, Kanazawa, Ishikawa, Japan, Tokyo Medical and Dental
University, Tokyo, Japan.
Source:
"Genotoxic Stress Abrogates Renewal of Melanocyte Stem Cells by
Triggering Their Differentiation." Publishing in Cell 137,
1088-1099, June 12, 2009. DOI 10.1016/j.cell.2009.03.037, a Cell Press
publication.