Researchers discovered that the protein Musashi-2 (Msi2) regulates bulk and metabolic processes in skeletal muscle.
The study was published in the journal 'The FASEB Journal.'
They looked at mice that had the Msi2 gene knocked out and discovered that they had less muscle mass because they had fewer type 2a muscle fibres. Myoglobin and mitochondrial function were similarly decreased. Type 2a fibres respond sensitively to training and sickness; understanding their modulation will be useful in developing new therapeutics.
The responsiveness of skeletal muscle fibres is absolutely remarkable. Training allows us to drastically increase muscle growth, strength, and endurance.
Muscles can atrophy as a result of age or prolonged periods of inactivity. Not only is that unpleasant for getting around, but it can also lead to a variety of other ailments. Scientists do not yet fully understand the mechanism by which muscle mass and strength are regulated.
A team led by Assistant Professor Yasuro Furuichi of Tokyo Metropolitan University has now discovered a critical piece of the jigsaw. They previously revealed that Musashi-2 (Msi2), a protein identified in nerve cells, was also expressed in skeletal muscle tissue.
Muscular atrophy also resulted in a decrease in Msi2 expression. They opted to look into Msi2 further because they suspected it played a more particular role in muscle fibre growth.
First, they isolated muscle fibres from nerves, blood arteries, and fat cells using enzymes on mouse muscle tissue. Msi2 was found to be expressed from muscle fibres, according to analysis. Furthermore, when they looked at fibres obtained from calf muscles, they discovered that Msi2 was most strongly expressed in type 1 or "slow" fibres, which had more endurance but less explosive power than type 2 or "fast" fibres.
The researchers also examined mice with the Musashi-2 protein gene intentionally "knocked out." They discovered that Msi2 deletion mice's calf muscles had much less bulk, a white colour, and decreased strength. Under a microscope, they discovered that the decrease in mass was caused by a decrease in the amount of type 2a fibres, a form of "fast" fibre with some of the endurance of "slow" fibres.
They also discovered that Msi2 deletion mice had a reduced ability to metabolise carbohydrates, which is similar to diabetes. There were fewer myoglobin and mitochondria, both of which are required for cell energy production.
The defect could be "fixed" by producing Msi2 in "fast" fibres, restoring both myoglobin and mitochondrial protein indicators. This demonstrates how Msi2 affects the amount of different types of fibre in skeletal muscle tissue by regulating proteins involved in sugar metabolism.
Type 2a fibres are especially responsive to training and deteriorate rapidly with age. This makes any understanding of how they are regulated a significant step forward in finding targets for new medicines to battle muscle atrophy and establishing training programmes to improve muscular strength.
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