Good pickup on Sunday… — Steve Coles
At 12:34 PM 9/7/2014, you wrote:
http://ift.tt/Wv61GX: Deborah Robison
Sanford-Burnham Medical Research Institute
“Researchers Discover a Key
to Making New Muscles”
A new study finds that cyclic bursts of a STAT3
replenish muscle stem cells and promote their differentiation into
muscle fibers. The findings are an important step toward developing
and maintaining new muscle to treat muscle diseases. IMAGE: This image depicts normal muscle (left) and muscle from
Muscular Dystrophy (right).
Click here for more information.
September 7, 2014; La Jolla, CA (Sanford-Burnham) — Researches
at Sanford-BurnhamnMedical Research Institute have developed a
novel technique to promote tissue repair in damaged muscles. The
technique also creates a sustainable pool of muscle stem cells
needed to support multiple rounds of muscle repair. The study,
published September 7th in Nature Medicine, provides promise for
a new therapeutic approach to treating the millions of people
suffering from muscle diseases, including those with muscular
dystrophies and muscle wasting associated with cancer and aging.
There are two important processes that need to happen
skeletal-muscle health. First, when muscle is damaged by injury or
degenerative disease such as muscular dystrophy, muscle stem
cells — or satellite cells — need to differentiate into mature muscle
cells to repair injured muscles. Second, the pool of satellite
cells needs to be replenished so there is a supply to repair muscle
in case of future injuries. In the case of muscular dystrophy, the
chronic cycles of muscle regeneration and degeneration that involve
satellite-cell activation exhaust the muscle stem-cell pool to the
point of no return.
“Our study found that by introducing an inhibitor
of the STAT3
protein in repeated cycles, we could alternately replenish the pool
of satellite cells and promote their differentiation into muscle
fibers,” said Alessandra Sacco, Ph.D., Assistant Professor in the
Development, Aging, and Regeneration Program at Sanford-Burnham.
“Our results are important because the process works in mice and in
human muscle cells.”
“Our next step is to see how long we can extend
pattern, and test some of the STAT3 inhibitors currently in
clinical trials for other indications such as cancer, as this could
accelerate testing in humans,” added Sacco.
“These findings are very encouraging. Currently,
there is no cure
to stop or reverse any form of muscle-wasting disorders — only
medication and therapy that can slow the process,” said Vittorio
Sartorelli, M.D., Chief of the Laboratory of Muscle Stem Cells and
Gene Regulation and Deputy Scientific Director at the National
Institute of Arthritis and Musculoskeletal and Skin Diseases
(NIAMS). “A treatment approach consisting of cyclic bursts of
STAT3 inhibitors could potentially restore muscle mass and function
in patients, and this would be a very significant breakthrough.”
Revealing the mechanism of STAT3
STAT3 (signal transducer and activator of transcription 3)
protein that activates the transcription of genes in response to IL-6,
a signaling protein released by cells in response to injury and
inflammation. Prior to the study, scientists knew that STAT3 played
a complex role in skeletal muscle, promoting tissue repair in some
instances and hindering it in others. But the precise mechanism of
how STAT3 worked was a mystery.
The research team first used normally aged mice and
mice models of
a form of muscular dystrophy that resembles the human disease to
see what would happen if they were given a drug to inhibit STAT3.
They found that the inhibitor initially promoted satellite-cell
followed by differentiation of the satellite cells into muscle fibers.
When they injected the STAT3 inhibitor every seven days for 28 days,
they found an overall improvement in skeletal-muscle repair, and an
increase in the size of muscle fibers.
“We were pleased to find that we achieved similar
results when we
performed the experiments in human muscle cells,” said Sacco.
have discovered that by timing the inhibition of STAT3 — like an
“on/off” light switch — we can transiently expand the
population followed by their differentiation into mature muscle
L. Stephen Coles, M.D., Ph.D., Cofounder
Los Angeles Gerontology Research GroupE-mail: email@example.comE-mail: