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Scientists discover clues to muscle stem cell functions by wwy yrj
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Scientists discover clues to muscle stem cell functions by WWY YRJ
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| Article Posted: 11/21/2012 |
| Article Views: 202 |
| Articles Written: 1412 - MORE ARTICLES FROM THIS AUTHOR |
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Scientists discover clues to muscle stem cell functions |
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The study, led by Julie D. Saba, MD, PhD, senior scientist atChildren's Hospital Oakland Research Institute (CHORI), shows thata lipid signaling molecule called sphingosine-1-phosphate or"S1P" can trigger an inflammatory response thatstimulates the muscle stem cells to proliferate and assist inmuscle repair. It further shows that mdx mice, which have a diseasesimilar to Duchenne Muscular Dystrophy, exhibit a deficiency ofS1P, and that boosting their S1P levels improves muscleregeneration in these mice. A research report describing the studyfindings will be published online on May 14, 2012 in the journal Public Library of Science ONE ( PLoS ONE ).
Skeletal muscle is the biggest "organ" system of thehuman body. It is important for all human activity. Muscles can beinjured by trauma, inactivity, aging and a variety of inheritedmuscle diseases. Importantly however, skeletal muscle is one of thefew tissues of the human body that has the potential to fullyrepair itself after injury. The ability of muscles to regeneratethemselves is attributed to the presence of a form of adult stemcells called "satellite cells" that are essential formuscle repair.
Normally, satellite cells lie quietly at theperiphery of the muscle fiber and do not grow, move or becomeactivated. However, after muscle injury, these stem cells"wake up" through unclear mechanisms and fuse with theinjured muscle, stimulating a complicated process that results inthe rebuilding of a healthy muscle fiber. S1P is a lipid signaling molecule that controls the movement andproliferation of many human cell types. Other scientists had shownpreviously that S1P can activate satellite cells, but they did notknow how this occurred. "We have been studying S1P signaling for many years,"states Dr.
Saba. "In 2003, we published a report demonstratingthat fruit fly mutants with defective S1P metabolism were unable tofly because they developed a muscle disease or "myopathy"that led to degeneration of their flight muscles. Based on thatobservation, I became convinced that S1P signaling played animportant role in muscle stability and homeostasis, not just inflies but in mammals, including humans." Dr. Saba's team has discovered how S1P is able to "wakeup" the stem cells at the time of injury. It involves theability of S1P to activate S1P receptor 2, one of its five cellsurface receptors, leading to downstream activation of aninflammatory pathway controlled by a transcription factor calledSTAT3.
They showed that S1P is rapidly produced in the muscleimmediately after injury, leading to an S1P "signal."S1P, acting through S1P receptor 2, leads to activation of STAT3,resulting in changes in gene expression that cause the satellitecell to leave its "sleeping" state and start toproliferate and assist in muscle repair. "These findings are important especially for certain musclediseases or "myopathies" that can affect children,"states Dr. Saba. The most common and one of the most severemyopathies is Duchenne Muscular Dystrophy, a disease that affectsyoung boys and often leads to death from respiratory and heartfailure in a patient's twenties.
Although patients with DuchenneMuscular Dystrophy start out life with enough satellite cells torepair the patients' degenerating muscles, over time the satellitecells fail to keep up with the rate of muscle degeneration."We found that mdx mice, which have a disease similar toDuchenne Muscular Dystrophy, are deficient in S1P. We were able toincrease the S1P levels in the mice using a drug that blocks S1Pbreakdown. This treatment increased the number of satellite cellsin the muscles and improved the efficiency of muscle regenerationafter injury." If these findings are also found to be true in humans with DuchenneMuscular Dystrophy, it may be possible to use similar approaches toboost S1P levels in order to improve satellite cell function andmuscle regeneration in patients with the disease. Drugs that blockS1P metabolism and boost S1P levels are now being tested for thetreatment of other human diseases including rheumatoid arthritis.If these studies prove to be relevant in Duchenne patients, it maybe possible to use the same drugs to improve muscle regeneration inthese patients. Alternatively, new agents that can specificallyactivate S1P receptor 2 could also be beneficial in recruitingsatellite cells and improving muscle regeneration in musculardystrophy and potentially other diseases of muscle.
This work was supported by grants from the Muscular DystrophyAssociation, the National Institutes of Health and a fellowshipaward from the California Institute of Regenerative Medicine. I am Apparel writer, reports some information about formal mens suits , black denim shorts.
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