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Transcriptomic analysis of muscle-resident fibro-adipogenic progenitor cells

ABSTRACT: Transcriptomic analysis of muscle-resident fibro-adipogenic progenitor cells

PROVIDER: PRJNA1037514 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26768100.fastq.gz	Fastqsanger.gz
	SRR26768200.fastq.gz	Fastqsanger.gz
	SRR26768300.fastq.gz	Fastqsanger.gz
	SRR26768400.fastq.gz	Fastqsanger.gz
	SRR26768500.fastq.gz	Fastqsanger.gz

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Transcriptomic analysis of muscle-resident fibro-adipogenic progenitor cells

Project description:We used single cell RNA-sequencing analysis to analyze the transcriptomic heterogeneity of fibro-adipogenic progenitors in skeletal muscle

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Project description:In human dystrophies, the progressive muscle wasting is exacerbated by ectopic deposition of fat and fibrous tissue originating from fibro/adipogenic progenitors (FAPs). In degenerating muscles, the ability of these cells to adjuvate a successful healing is attenuated and FAPs aberrantly expand and differentiate into adipocytes and fibroblasts. Thus, arresting the fibroadipogenic fate of FAPs, without affecting their physiological role, represents a valuable therapeutic strategy for patients affected by muscle diseases. Here, using a panel of adipose progenitor cells including human-derived FAPs coupled with pharmacological perturbations and proteome profiling, we report that LY2090314 interferes with a genuine adipogenic program acting as WNT surrogate for the stabilization of a competent -catenin transcriptional complex. To predict the beneficial impact of LY2090314 in limiting ectopic deposition of fat in human muscles, we combined the Poly-Ethylene-Glycol-Fibrinogen biomimetic matrix with these progenitor cells to create a miniaturized 3D model of adipogenesis. Using this scalable system, we demonstrated that a two-digit nanomolar dose of this compound is effective to repress adipogenesis in a higher 3D scale, thus offering a concrete proof for the use of LY2090314 to limit FAP-derived fat infiltrates in dystrophic muscles.

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Project description:The purpose of this study is to investigate how melatonin-influenced promyogenic factor secreted from fibro-adipogenic progenitors (FAPs) regulate muscle regeneration and muscle cell fusion during muscle repair. We highlighted the role of melatonin in regulating crosstalk between muscle stem cells and FAPs during muscle regeneration. Mice that were treated with melatonin exhibited improved muscle regeneration and reduced intramuscular fat deposition, which were associated with enhanced myogenesis, remodeled lipid metabolism and reduced immune cell infiltration. Notably, melatonin did not exert positive effects on cell fusion and myotube formation during differentiation. Interestingly, melatonin repressed fibro-adipogenic progenitor (FAP) adipogenesis in a dose-dependent manner in vitro. Furthermore, melatonin treatment enhanced the pro-myogenic effects of FAPs, which stimulated GDF10 secretion to promote muscle cell fusion and induce myotube hypertrophy.

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