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

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

PROVIDER: PRJNA554574 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9681134_1.fastq.gz	Fastqsanger.gz
	SRR9681134_2.fastq.gz	Fastqsanger.gz
	SRR9681135_1.fastq.gz	Fastqsanger.gz
	SRR9681135_2.fastq.gz	Fastqsanger.gz
	SRR9681136_1.fastq.gz	Fastqsanger.gz

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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: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.

2020-01-01 | GSE134251 | 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 (scRNA-seq)

2019-09-05 | GSE134540 | GEO

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

| PRJNA554568 | ENA

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)

| PRJNA554573 | 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)

| PRJNA555526 | ENA

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-09-06 | GSE134253 | GEO

Jakyak-gamcho-tang ameliorates dexamethasone-induced muscle atrophy and muscle dysfunction

Project description:Jakyak-gamcho-tang ameliorates dexamethasone-induced muscle atrophy and muscle dysfunction

| PRJNA945385 | ENA

Jakyak-gamcho-tang ameliorates dexamethasone-induced muscle atrophy and muscle dysfunction [C2C12]

Project description:Jakyak-gamcho-tang ameliorates dexamethasone-induced muscle atrophy and muscle dysfunction [C2C12]

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Mitofusin 2 expression in muscle decreases during aging and generates a gene signature characteristic of aged muscle

Project description:Mitochondrial fusion and fission proteins regulate mitochondrial quality control and mitochondrial metabolism. In turn, mitochondrial dysfunction is associated with aging, although its causes are still under debate. Here, we show that aging is characterized by a progressive reduction of Mitofusin 2 (Mfn2) in mouse skeletal muscle and that skeletal muscle Mfn2 ablation in mice generates a gene signature linked to aging. Furthermore, muscle Mfn2-deficient mice show unhealthy aging characterized by altered metabolic homeostasis and sarcopenia. Mfn2 deficiency impairs mitochondrial quality control, which contributes to an exacerbated age-related mitochondrial dysfunction. Surprisingly, aging-induced Mfn2 deficiency triggers a ROS-dependent retrograde signaling pathway through induction of HIF1 transcription factor and BNIP3. This pathway ameliorates mitochondrial autophagy and minimizes mitochondrial damage. Our findings reveal that repression of Mfn2 in skeletal muscle during aging is determinant for the loss of mitochondrial quality, contributing to age-associated metabolic alterations and loss of muscle fitness. Quadriceps muscle from four mice per genotype were used (Control young (6 month-old), Mfn2KO young (6-month-old), control old (22-month-old) and Mfn2KO old (22-month-old)

2016-08-08 | E-GEOD-71501 | biostudies-arrayexpress

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