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Muscle-secreted G-CSF as a metabolic niche factor ameliorates loss of muscle stem cell in aged mice

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE134253 | GEO | 2019/09/06

REPOSITORIES: GEO

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Muscle-secreted G-CSF as a metabolic niche factor ameliorates loss of muscle stem cell in aged mice (scRNA-seq)

Project description:Function and number of muscle stem cells (satellite cells, SCs) declines with muscle aging. Although SCs are heterogeneous and different subpopulations have been identified, it remains unknown if a specific subpopulation of muscle SCs selectively decreases during aging. Here, we find Pax7Hi cells are dramatically reduced in aged mice and this aged-dependent loss of Pax7Hi cells is metabolically mediated by myofiber-secreted granulocyte-colony stimulating factor G-CSF as the Pax7Hi SCs are replenished by exercise-induced G-CSF in aged mice. Mechanistically, we show that transcription of G-CSF (Csf3) gene in myofibers is regulated by MyoD in a metabolism-dependent manner and the myofibers-secreted G-CSF acts as a metabolic niche factor required for establishing and maintaining the Pax7Hi SC subpopulation in adult and physiological aged mice by promoting the asymmetric division of Pax7Hi and Pax7Mi SCs. Together, our findings uncover a metabolic niche role of muscle metabolism in regulating Pax7 SC heterogeneity in mice.

2019-09-05 | GSE134540 | GEO

Muscle-secreted G-CSF as a metabolic niche factor ameliorates loss of muscle stem cell in aged mice (RNA-seq)

2019-09-05 | GSE134252 | GEO

Muscle-secreted G-CSF as a metabolic niche factor ameliorates loss of muscle stem cell in aged mice (ChIP-seq)

2020-01-01 | GSE134251 | GEO

Muscle-secreted granulocyte colony-stimulating factor functions as metabolic niche factor ameliorating loss of muscle stem cells in aged mice.

Project description:The function and number of muscle stem cells (satellite cells, SCs) decline with muscle aging. Although SCs are heterogeneous and different subpopulations have been identified, it remains unknown whether a specific subpopulation of muscle SCs selectively decreases during aging. Here, we find that the number of SCs expressing high level of transcription factor Pax7 (Pax7Hi ) is dramatically reduced in aged mice. Myofiber-secreted granulocyte colony-stimulating factor (G-CSF) regulates age-dependent loss of Pax7Hi cells, as the Pax7Hi SCs are replenished by exercise-induced G-CSF in aged mice. Mechanistically, we show that transcription of G-CSF (Csf3) gene in myofibers is regulated by MyoD in a metabolism-dependent manner. Furthermore, myofiber-secreted G-CSF acts as a metabolic niche factor required for establishing and maintaining the Pax7Hi SC subpopulation in adult and physiological aged mice by promoting the asymmetric division of Pax7Hi and Pax7Mi SCs. Together, our findings uncover that muscles provide a metabolic niche regulating Pax7 SC heterogeneity in mice.

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Muscle-secreted G-CSF as a metabolic niche factor ameliorates loss of muscle stem cell in aged mice

Project description:Muscle-secreted G-CSF as a metabolic niche factor ameliorates loss of muscle stem cell in aged mice

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Muscle-secreted G-CSF as a metabolic niche factor ameliorates loss of muscle stem cell in aged mice (ChIP-seq)

Project description:Muscle-secreted G-CSF as a metabolic niche factor ameliorates loss of muscle stem cell in aged mice (ChIP-seq)

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Muscle-secreted G-CSF as a metabolic niche factor ameliorates loss of muscle stem cell in aged mice (RNA-seq)

Project description:Muscle-secreted G-CSF as a metabolic niche factor ameliorates loss of muscle stem cell in aged mice (RNA-seq)

| PRJNA554574 | ENA

Muscle-secreted G-CSF as a metabolic niche factor ameliorates loss of muscle stem cell in aged mice (scRNA-seq)

Project description:Muscle-secreted G-CSF as a metabolic niche factor ameliorates loss of muscle stem cell in aged mice (scRNA-seq)

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Induction of muscle stem cell quiescence by the secreted niche factor Oncostatin M.

Project description:The balance between stem cell quiescence and proliferation in skeletal muscle is tightly controlled, but perturbed in a variety of disease states. Despite progress in identifying activators of stem cell proliferation, the niche factor(s) responsible for quiescence induction remain unclear. Here we report an in vivo imaging-based screen which identifies Oncostatin M (OSM), a member of the interleukin-6 family of cytokines, as a potent inducer of muscle stem cell (MuSC, satellite cell) quiescence. OSM is produced by muscle fibers, induces reversible MuSC cell cycle exit, and maintains stem cell regenerative capacity as judged by serial transplantation. Conditional OSM receptor deletion in satellite cells leads to stem cell depletion and impaired regeneration following injury. These results identify Oncostatin M as a secreted niche factor responsible for quiescence induction, and for the first time establish a direct connection between induction of quiescence, stemness, and transplantation potential in solid organ stem cells.

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The aged niche disrupts muscle stem cell quiescence.

Project description:The niche is a conserved regulator of stem cell quiescence and function. During ageing, stem cell function declines. To what extent and by what means age-related changes within the niche contribute to this phenomenon are unknown. Here we demonstrate that the aged muscle stem cell niche, the muscle fibre, expresses Fgf2 under homeostatic conditions, driving a subset of satellite cells to break quiescence and lose their self-renewing capacity. We show in mice that relatively dormant aged satellite cells robustly express sprouty?1 (Spry1), an inhibitor of fibroblast growth factor (FGF) signalling. Increasing FGF signalling in aged satellite cells under homeostatic conditions by removing Spry1 results in the loss of quiescence, satellite cell depletion and diminished regenerative capacity. Conversely, reducing niche-derived FGF activity through inhibition of Fgfr1 signalling or overexpression of Spry1 in satellite cells prevents their depletion. These experiments identify an age-dependent change in the stem cell niche that directly influences stem cell quiescence and function.

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