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MEDICAL MUSCLES AND MUSCULAR :
MEDICAL: TISSUE REPAIR :
MEDICAL: GENETICS :
MEDICAL: RESEARCH:
NIH Scientists Identify Gene that Could Hold the Key to Muscle Repair
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Date: Fri, 15 Apr 2011 10:41:12 -0400
From: "NIH OLIB (NIH/OD)" <[log in to unmask]>
To: [log in to unmask]
Subject: NIH Scientists Identify Gene that Could Hold the Key
to Muscle Repair
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U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH NIH News
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National Institute of Arthritis and Musculoskeletal and Skin Diseases
(NIAMS)
http://www.niams.nih.gov/
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For Immediate Release: Friday, April 15, 2011
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CONTACT:
Trish Reynolds
301-496-8190
e-mail:
[log in to unmask]
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NIH SCIENTISTS IDENTIFY GENE THAT COULD HOLD THE KEY TO MUSCLE REPAIR
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Researchers have long questioned why patients with Duchenne muscular
dystrophy (DMD) tend to manage well through childhood and adolescence, yet
succumb to their disease in early adulthood, or why elderly people who
lose muscle strength following bed rest find it difficult or impossible to
regain. Now, researchers at the National Institute of Arthritis and
Musculoskeletal and Skin Diseases (NIAMS), part of the National Institutes
of Health, are beginning to find answers in a specialized population of
cells called satellite cells. Their findings, reported in the journal
Genes & Development, suggest a potential therapeutic target for conditions
where muscle deterioration threatens life or quality of life.
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Key to the development of skeletal muscle of the embryo and fetus,
satellite cells continue to actively increase muscle mass through infancy.
After that, they decrease in number and become quiescent, or inactive,
until they are activated by injury or degeneration to proliferate. The
process, which enables the body to repair damaged muscle, works quite well
- to a point, says Vittorio Sartorelli, M.D., senior investigator in the
NIAMS Laboratory of Muscle Stem Cells and Gene Regulation and lead author
of the study.
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For example, when a young person experiences muscle loss after a period of
inactivity, muscle rebuilds as soon as activity is resumed. However, in
the elderly, muscles lose that capacity. Similarly, in patients with DMD,
the initial phases of muscle degeneration are effectively counteracted by
the ability of satellite cells to regenerate.
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"That is why people can survive until they are 20 years old without much
of a problem, but, at a certain point, satellite cells stop
proliferating," said Dr. Sartorelli. "That is the point at which the
patient will start developing weakness and problems that will ultimately
lead to death."
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Suspecting a genetic switch that might turn off satellite cell
proliferation in these circumstances, the scientists looked to a gene
called Ezh2, known to keep the activity of other genes in check. When they
genetically inactivated Ezh2 in satellite cells of laboratory mice, the
mice failed to repair muscle damage caused by traumatic injury - satellite
cells could not proliferate.
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Ezh2 expression is known to decline during aging, and the new research in
mice suggests that therapies to activate Ezh2 and promote satellite cell
proliferation might eventually play a role in treating degenerative muscle
diseases.
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"We will not be able to cure the muscular dystrophies with this approach
because the mutation in the gene that causes the diseases would remain.
But certainly, if we can extend the period in which the satellite cells
proliferate and compensate for the underlying defect, we might increase
the lifespan of people with muscular dystrophy. We could certainly
increase their quality of life," said Dr. Sartorelli.
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Likewise, in the elderly, tweaking the gene in satellite cells would not
increase their lifespan, but could increase their quality of life by
helping to prevent falls and enabling them to move and walk better and go
about their daily activities.
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Dr. Sartorelli cautions that while the identification of Ezh2's role is a
crucial step, any therapies are still many years away.
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For more information about the NIAMS Laboratory of Muscle Stem Cells and
Gene Regulation, visit
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http://www.niams.nih.gov/Research/Ongoing_Research/
Branch_Lab/Muscle_Stem_Cells_and_Gene_Regulation/default.asp
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The mission of the National Institute of Arthritis and Musculoskeletal and
Skin Diseases (NIAMS), a part of the U.S. Department of Health and Human
Services' National Institutes of Health (NIH), is to support research into
the causes, treatment, and prevention of arthritis and musculoskeletal and
skin diseases; the training of basic and clinical scientists to carry out
this research; and the dissemination of information on research progress
in these diseases. For more information about the NIAMS, call the
information clearinghouse at
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(301) 495-4484
or
(877) 22-NIAMS (free call)
or visit the NIAMS website at
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http://www.niams.nih.gov
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About the National Institutes of Health (NIH): NIH, the nation's medical
research agency, includes 27 Institutes and Centers and is a component of
the U.S. Department of Health and Human Services. NIH is the primary
federal agency conducting and supporting basic, clinical, and
translational medical research, and is investigating the causes,
treatments, and cures for both common and rare diseases. For more
information about NIH and its programs, visit
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http://www.nih.gov
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REFERENCE:
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Juan AH, Derfoul A, Feng X, Ryall JG, Dell'Orso S, Pasut A, Zare H, Simone
JM, Rudnicki MA, Sartorelli V.
Polycomb EZH2 controls self-renewal and safeguards the transcriptional
identity of skeletal muscle stem cells.
Genes Dev. 25:789-794.
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##
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This NIH News Release is available online at:
http://www.nih.gov/news/health/apr2011/niams-15.htm
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Sincerely,
David Dillard
Temple University
(215) 204 - 4584
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http://daviddillard.businesscard2.com
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