Tokyo [Japan], September 9 : Musashi-2 (Msi2) is a major player in the control of skeletal muscle metabolism and mass, according to research from Tokyo Metropolitan University. They observed lower muscle mass in mice that had the Msi2 gene knocked out due to a lack of type 2a muscular fibres.
Additionally decreased were mitochondria and myoglobin. Type 2a fibres are sensitive to disease and training, and future treatments will benefit from understanding how they are regulated.
The responsiveness of skeletal muscle fibres is absolutely remarkable. We may greatly increase our muscle mass, strength, and endurance through training. On the other hand, muscle can also atrophy with time and/or prolonged periods of inactivity.
That not only makes it difficult to move around, but it can also lead to a variety of other diseases. However, scientists are still unsure of the precise process by which muscle size and strength are controlled.
Now, a team led by Assistant Professor Yasuro Furuichi from Tokyo Metropolitan University have emerged with a key part of the puzzle. In previous work, they found that Musashi-2 (Msi2), a protein originally discovered in nerve cells, was also expressed in skeletal muscle tissue.
Muscular atrophy also led to a decrease in the expression of Msi2. Suspecting that Msi2 had a more specific role in the development of muscle fibres, they decided to take a closer look.
Firstly, they took muscle tissue from mice and applied enzymes to isolate the muscle fibres from nerves, blood vessels and fat cells. The analysis confirmed that Msi2 was indeed being expressed from the muscle fibres themselves.
Furthermore, on looking at fibres taken from calf muscles, they found Msi2 was most strongly expressed in type 1 or “slow” fibres, fibres with more endurance but less explosive power than their type 2 or “fast” counterparts.
The team also looked at mice with the gene coding for the Musashi-2 protein artificially “knocked out”. They found that the calf muscles of Msi2 knockout mice had significantly reduced mass, with a whitish colour, and less strength.
On looking at fibre types under a microscope, they found that the reduction in mass was due to a drop in the number of type 2a fibres, a type of “fast” fibre that has some of the endurance of “slow” fibres.
They also noted that Msi2 knockout mice were less able to metabolize sugars, much like in diabetes. There were fewer myoglobin and mitochondria, both vital to producing energy in cells.
The problem could be “fixed” by expressing Msi2 in “fast” fibres, restoring both myoglobin and protein markers for mitochondria. This highlights how Msi2 regulates proteins associated with sugar metabolism and effectively controls the proportion of different types of fibre in skeletal muscle tissue.
Type 2a fibres are particularly responsive to training and atrophy easily with age. This makes any insights into how they are regulated a key advance in identifying targets for new therapies to combat muscle decline, as well as developing training regimens to improve muscle strength.
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