Regulation of muscle hypertrophy through granulin: Relayed communication among mesenchymal progenitors, macrophages, and satellite cells

Skeletal muscle stem cells (MuSCs) display distinct behavior crucial for tissue maintenance and repair. Upon activation, MuSCs exhibit distinct modes of division: symmetric division, facilitating either self-renewal or differentiation, and asymmetric division, which dictates divergent cellular fates. This review explores the nuanced dynamics of MuSC division and the molecular mechanisms governing this behavior. Furthermore, it introduces a novel phenomenon observed in a subset of MuSCs under hypertrophic stimuli termed division-independent differentiation. Insights into the underlying mechanisms driving this process are discussed, alongside its broader implications for muscle physiology.

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Decreased number of satellite cells-derived myonuclei in both fast- and slow-twitch muscles in HeyL-KO mice during voluntary running exercise

Iwamori,

Kubota,

Kodama

et al. 2024

Preprint

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Background Skeletal muscles possess unique abilities known as adaptation or plasticity. When exposed to external stimuli, such as mechanical loading, both myofiber size and myonuclear number increase. Muscle stem cells, also known as muscle satellite cells (MuSCs), play vital roles in these changes. HeyL, a direct target of Notch signaling, is crucial for efficient muscle hypertrophy because it ensures MuSC proliferation in surgically overloaded muscles by inhibiting the premature differentiation. However, it remains unclear whether HeyL is essential for MuSC expansion in physiologically loaded muscles. Additionally, the influence of myofiber type on the requirement for HeyL in MuSCs within loaded muscles remains unclear. Methods We used a voluntary wheel running model and HeyL-knockout mice to investigate the impact of HeyL deficiency on MuSC-derived myonuclei, MuSC behavior, muscle weight, myofiber size, and myofiber type in the running mice. Results The number of new MuSC-derived myonuclei was significantly lower in both slow-twitch soleus and fast-twitch plantaris muscles from exercised HeyL-knockout mice than in control mice. However, exercised HeyL-knockout mice exhibited similar responses to control mice regarding myofiber size and type. Conclusions HeyL expression is crucial for MuSC expansion during physiological exercise in both slow and fast muscles. Nevertheless, the absence of HeyL did not affect the increased myofiber size or alteration of myofiber types, suggesting that MuSCs are not required in the wheel-running model because of the low degree of hypertrophy compared with that in surgically overloaded models.

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Regulation of muscle hypertrophy through granulin: Relayed communication among mesenchymal progenitors, macrophages, and satellite cells

Cited by 3 publications

References 67 publications

Advances in CRISPR-Cas systems for epigenetics

Advances in CRISPR-Cas systems for epigenetics

Satellite cell dynamics during skeletal muscle hypertrophy

Decreased number of satellite cells-derived myonuclei in both fast- and slow-twitch muscles in HeyL-KO mice during voluntary running exercise

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