The absence of PRMT1 increases muscle stem cell expansion

What is it about?

Throughout one’s lifetime, muscles are injured upon constant usage in day to day activities. Damaged cells within the injured muscle require efficient replacement in order to improve the healing process; this process is called muscle regeneration. Muscle regeneration requires the presence of quiescent muscle stem cells that will ensure both the maintenance of the pool and the regeneration in response to injury. We identified the protein PRMT1, an enzyme catalyzing arginine methylation, as a key regulator of muscle stem cell fate. Using mouse as an animal model, we demonstrated that the specific ablation of PRMT1 in muscle stem cells prevents proper muscle regeneration but increases muscle stem cell expansion.

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Why is it important?

Understanding how injured muscles undergo regeneration is a major area of interest in medicine as it could help develop treatments for many muscular diseases. A current challenge in regenerative medicine is to efficiently expand the muscle stem cells responsible for muscle regeneration. In this article, we found that depleting PRMT1 in muscle stem cells lead to a significant increase of the cell population expansion. We also found that the permanent depletion of the PRMT1 was preventing proper muscle regeneration. Finding the balance to control muscle stem cell fate and expansion is key to help develop stem cell based therapies in order to treat muscle dystrophies, and to prevent or delay aged-related muscle mass (sarcopenia).

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