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Understanding How Stem Cells React May Mean New Therapies for Damaged Muscles

Posted on December 29, 2017

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Researchers from the Sanford Burnham Prebys Medical Discovery Institute have found that muscle cells respond differently to aging than injury.

The research, published in Cell Stem Cell, is critical for the development of future treatments and therapies to restore muscle tissue lost under a variety of circumstances such as normal wear, aging, injury or illness.

The SBP study is the first study of its kind to look at and measure how muscle cells respond differently to the stress of aging and injury.

Muscle Matters

Muscle tissue loss due to aging is a condition known as sarcopenia. Sarcopenia occurs most frequently after the age of 40, and the consequences of the condition include muscle weakness, loss of stamina and decreased mobility. In serious cases, complete immobility may occur.

Sarcopenia also results in disability and increased mortality rates.

Muscle injuries can also result in limited function, complete dysfunction and loss of mobility. Other side effects of muscle injuries include scar tissue, pain and chronic inflammation.

How Stem Cells Repair Muscle Damage

Adult muscle stem cells are found in the fibers of the muscle tissue, where they lay dormant until needed for repairs. The adult muscle stem cell pool is made up of a diverse group of cells.

Adult muscle stem cells must self-renew to maintain their numbers to be ready to repair damaged tissue and be able to differentiate into different muscle tissue types.

To repair damaged tissue, adult stem cells regenerate themselves into two daughter cells during the process of cell division. One daughter cell develops the type of muscle tissue needed for repair, while the other cell maintains the stem cell pool for future repairs.

“When the body experiences tissue damage for any reason, the damaged tissue puts off a call for help using growth factors. These growth factors wake up the sleeping adult stem cells and tell them what to do,” said Dr. Joel Singer.

Singer is a New York physician who treats patients with muscle damage caused by aging, injury, trauma and autoimmune conditions.

Potential for New Treatments

Using in vivo multilineage technology to trace how adult muscle stem cells regenerate and differentiate, the SBP study authors found that adult muscle stem cells react differently to different types of damage.

In the case of muscle tissue damage caused by aging, researchers found that the adult muscle stem cell pool maintains its diversity instead of differentiating to one type of tissue.

The SBP researchers also created an injury in muscle tissue to see how the adult muscle stem cells reacted. They found that the adult muscle stem cell pool becomes less diverse as the cells rush to differentiate and heal the type of tissue that is injured.

The authors of the SBP study hope that their research could lead to a new understanding of how the adult muscle stem cells react to stress caused by factors other than injury. The hope is that this work may lead to new treatments for other muscular diseases, such as muscular dystrophy, myositis and amyotrophy.

“Although muscular dystrophy usually causes weakness in the limbs, over time this weakness can spread to other body areas, like the heart, lungs and intestines,” Singer said. “Understanding how the stem cells react in response to these stimuli may mean new ways to treat muscle weakness and injury, which could potentially change outcomes for patients with muscular dystrophy and other types of muscle conditions.”

Muscular dystrophy is a group of over 30 genetic conditions caused by genetic mutations that prevent the development of healthy muscle tissue. The most common type of muscular dystrophy is Duchenne Muscular Dystrophy.

Source:

Sanford-Burnham Prebys Medical Discovery Institute. “Researchers track muscle stem cell dynamics in response to injury and aging: Distinct differences found in how skeletal muscle stem cells cope with different stimuli.” ScienceDaily. ScienceDaily, 14 December 2017.

 

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