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Overloading MuSCs

ABSTRACT: Skeletal muscle possesses the ability to adapt its size in response to milieus, which is called plasticity. Overload like resistance training induces the increment of muscle mass called muscle hypertrophy. Muscle stem cells (also known as muscle stem cells) function to supply new nuclei for myofiber during the overload in muscle. Using compensatory hypertrophy in plantaris muscles, we isolated MuSCs from plantaris muscles 4 days after surgery. Control MuSCs were also prepared from sham plantaris muscles.

ORGANISM(S): Mus musculus

PROVIDER: GSE135903 | GEO | 2019/09/23

REPOSITORIES: GEO

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Overloading mesenchymal progenitors (FAPs)

Project description:Skeletal muscle possesses the ability to adapt its size in response to milieus, which is called plasticity. Resistance training induces the increment of muscle mass called muscle hypertrophy. Muscle stem cells (MuSC; also known as muscle stem cells) function to supply new nuclei for myofiber during the overload in muscle. We found that Yap1 and Taz in mesenchymal progenitors (also called FAPs) are critical for MuSC proliferation in overloaded muscles. We hypothsize that Yap1/Taz-dependent mesenchymal progenitors derived factor induces MuSC proliferation. In order to identify such factors, RNA-seq of overloaded FAPs were performed.

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Overloading mesenchymal progenitors (FAPs)

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Overloading MuSCs

Project description:Overloading MuSCs

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Expression data during plantaris muscle hypertrophy with/without satellite cells induced by synergist ablation in young adult Pax7-DTA mice

Project description:Global gene expression patterns were determined from microarray results from sham surgery or following 1 week of plantaris muscle hypertrophy induced by synergist ablation in young adult Pax7-DTA mice (4 months). Vehicle treated mice have their full complement of satellite cells; tamoxifen treated mice have had their satellite cells genetically depleted through Cre-loxP technology After sham surgery or 1 week of overload, Affymetrix chips (mouse430_2.0) were used with 1 Âµg of total RNA derived from a pooled sample of the right and left plantaris muscles from 11 animals.

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Changes in gene expression after mechanical loading with and without satellite cell.

Project description:Skeletal muscle is a plastic tissue, adapting to different stimuli. Mechanical overload causes muscle hypertrophy and substantial changes in gene expression. We perform a time course analysis following synergistic ablation surgery to induce compensatory hypertrophy in the plantaris muscle in satellite cell depleted mice and wild-type mice. Microarray was used to determine the different expressed genes in skeletal muscle with or without satellite cell following mechanical overload.

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Expression data during plantaris muscle hypertrophy induced by synergist ablation in young adult mice

Project description:Global gene expression patterns were determined from microarray results on day 1, 3, 5, 7, 10 and 14 during plantaris muscle hypertrophy induced by synergist ablation in young adult mice (5 months). For each time point, two Affymetrix chips (Mouse Gene 1.0 ST) were used with 100 ng of total RNA derived from a pooled sample of either the right or left plantaris muscles from six animals.

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14d OV scRNA-seq

Project description:The goal of this project was to determine which mononuclear cell populations satellite cells communicate with throughout muscle during functional overload. Pooled mouse plantaris muscles from tamoxifen-treated Pax7-tdT mice were overloaded for 14 days, and a subset of mononuclear cells were submitted for sc-RNA-seq.

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Muscle Overload scRNA-seq

Project description:The goal of this project was to determine which mononuclear cell populations satellite cells communicate with throughout muscle during synergist ablation functional overload. Mouse plantaris muscles from tamoxifen-treated Pax7-tdT, tdT, and Pax7-DTA mice were overloaded for 4-14 days, and a subset of mononuclear cells were submitted for sc-RNA-seq.

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Senolytics rescue blunted muscle hypertrophy in old mice

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2022-05-29 | GSE195707 | GEO

Extracellular matrix remodelling is associated with muscle force increase in overloaded mouse plantaris muscle.

Project description:Aims: Transforming growth factor-β (TGF-β) signalling is thought to contribute to the remodelling of extracellular matrix (ECM) of skeletal muscle and to functional decline in patients with muscular dystrophies. We wanted to determine the role of TGF-β-induced ECM remodelling in dystrophic muscle. Methods: We experimentally induced the pathological hallmarks of severe muscular dystrophy by mechanically overloading the plantaris muscle in mice. Furthermore, we determined the role of TGF-β signalling on dystrophic tissue modulation and on muscle function by (i) overloading myostatin knockout (Mstn-/- ) mice and (ii) by additional pharmacological TGF-β inhibition via halofuginone. Results: Transcriptome analysis of overloaded muscles revealed upregulation predominantly of genes associated with ECM, inflammation and metalloproteinase activity. Histology revealed in wild-type mice signs of severe muscular dystrophy including myofibres with large variation in size and internalized myonuclei, as well as increased ECM deposition. At the same time, muscle weight had increased by 208% and muscle force by 234%. Myostatin deficiency blunted the effect of overload on muscle mass (59% increase) and force (76% increase), while having no effect on ECM deposition. Concomitant treatment with halofuginone blunted overload-induced muscle hypertrophy and muscle force increase, while reducing ECM deposition and increasing myofibre size. Conclusions: ECM remodelling is associated with an increase in muscle mass and force in overload-modelled dystrophic muscle. Lack of myostatin is not advantageous and inhibition of ECM deposition by halofuginone is disadvantageous for muscle plasticity in response to stimuli that induce dystrophic muscle.

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