AMPKα2 is a skeletal muscle stem cell intrinsic regulator of myonuclear accretion.

Autor:	Kneppers A; Institut NeuroMyoGène, CNRS UMR 5261, INSERM U1315, Université Claude Bernard Lyon 1, Lyon, France., Ben Larbi S; Institut NeuroMyoGène, CNRS UMR 5261, INSERM U1315, Université Claude Bernard Lyon 1, Lyon, France., Theret M; Institut NeuroMyoGène, CNRS UMR 5261, INSERM U1315, Université Claude Bernard Lyon 1, Lyon, France., Saugues A; Institut NeuroMyoGène, CNRS UMR 5261, INSERM U1315, Université Claude Bernard Lyon 1, Lyon, France., Dabadie C; Institut NeuroMyoGène, CNRS UMR 5261, INSERM U1315, Université Claude Bernard Lyon 1, Lyon, France., Gsaier L; Institut NeuroMyoGène, CNRS UMR 5261, INSERM U1315, Université Claude Bernard Lyon 1, Lyon, France., Ferry A; Myology Center of Research, Association of Myology Institute, INSERM UMRS974, Sorbonne Université, Paris, France.; Université Paris Cité, Paris, France., Rhein P; Nestlé Research, Société des Produits Nestlé S.A., EPFL Innovation Park, Lausanne, Switzerland.; School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne (EPFL), EPFL Innovation Park, Lausanne, Switzerland., Gondin J; Institut NeuroMyoGène, CNRS UMR 5261, INSERM U1315, Université Claude Bernard Lyon 1, Lyon, France., Sakamoto K; Nestlé Research, Société des Produits Nestlé S.A., EPFL Innovation Park, Lausanne, Switzerland.; Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Copenhagen, Denmark., Mounier R; Institut NeuroMyoGène, CNRS UMR 5261, INSERM U1315, Université Claude Bernard Lyon 1, Lyon, France.
Jazyk:	angličtina
Zdroj:	IScience [iScience] 2023 Oct 26; Vol. 26 (12), pp. 108343. Date of Electronic Publication: 2023 Oct 26 (Print Publication: 2023).
DOI:	10.1016/j.isci.2023.108343
Abstrakt:	Due to the post-mitotic nature of skeletal muscle fibers, adult muscle maintenance relies on dedicated muscle stem cells (MuSCs). In most physiological contexts, MuSCs support myofiber homeostasis by contributing to myonuclear accretion, which requires a coordination of cell-type specific events between the myofiber and MuSCs. Here, we addressed the role of the kinase AMPKα2 in the coordination of these events supporting myonuclear accretion. We demonstrate that AMPKα2 deletion impairs skeletal muscle regeneration. Through in vitro assessments of MuSC myogenic fate and EdU-based cell tracing, we reveal a MuSC-specific role of AMPKα2 in the regulation of myonuclear accretion, which is mediated by phosphorylation of the non-metabolic substrate BAIAP2. Similar cell tracing in vivo shows that AMPKα2 knockout mice have a lower rate of myonuclear accretion during regeneration, and that MuSC-specific AMPKα2 deletion decreases myonuclear accretion in response to myofiber contraction. Together, this demonstrates that AMPKα2 is a MuSC-intrinsic regulator of myonuclear accretion. Competing Interests: The authors declare no competing interests. (© 2023 The Authors.)
Databáze:	MEDLINE
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