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MuSC dysfunction contributes to dystrophic progression and impaired regeneration in the mdx mouse [bulk RNA-seq]

ABSTRACT: MuSC dysfunction contributes to dystrophic progression and impaired regeneration in the mdx mouse [bulk RNA-seq]

PROVIDER: PRJNA1116201 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29165003.fastq.gz	Fastqsanger.gz
	SRR29165004.fastq.gz	Fastqsanger.gz
	SRR29165005.fastq.gz	Fastqsanger.gz
	SRR29165006.fastq.gz	Fastqsanger.gz
	SRR29165007.fastq.gz	Fastqsanger.gz

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MuSC dysfunction contributes to dystrophic progression and impaired regeneration in the mdx mouse

Project description:MuSC dysfunction contributes to dystrophic progression and impaired regeneration in the mdx mouse

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MuSC dysfunction contributes to dystrophic progression and impaired regeneration in the mdx mouse [scRNA-seq]

Project description:MuSC dysfunction contributes to dystrophic progression and impaired regeneration in the mdx mouse [scRNA-seq]

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MuSC dysfunction contributes to dystrophic progression and impaired regeneration in the mdx mouse [scRNA-seq]

Project description:Duchenne muscular dystrophy (DMD) is a devastating disease characterized by progressive muscle wasting and limitation of life. In addition to the inherent weakness of dystrophin-deficient muscle, the dysfunction of resident muscle stem cells significantly contributes to disease progression. Using the mdx mouse model of DMD, we performed an in-depth characterization of disease progression and muscle stem cell (MuSC) function in dystrophin deficient skeletal muscle using immunohistology, isometric force measurements, transplantation assays, and transcriptomic analysis. Here, we performed single cell RNA-sequencing of wild-type (WT) and mdx myogenic cells before and 5-days following cardiotoxin injury.

2025-01-02 | GSE268314 | GEO

MuSC dysfunction contributes to dystrophic progression and impaired regeneration in the mdx mouse [bulk RNA-seq]

Project description:Duchenne muscular dystrophy (DMD) is a devastating disease characterized by progressive muscle wasting and limitation of life. In addition to the inherent weakness of dystrophin-deficient muscle, the dysfunction of resident muscle stem cells significantly contributes to disease progression. Using the mdx mouse model of DMD, we performed an in-depth characterization of disease progression and muscle stem cell (MuSC) function in dystrophin deficient skeletal muscle using immunohistology, isometric force measurements, transplantation assays, and transcriptomic analysis. Here, we performed bulk RNA-sequencing of wild-type (WT) and mdx myogenic cells in different conditions.

2025-01-02 | GSE268313 | GEO

MuSC dysfunction contributes to dystrophic progression and impaired regeneration in the mdx mouse

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

2025-01-02 | GSE268316 | GEO

HDAC inhibitors promote the pro-myogenic activity of Sca1-positive interstitial cells in regenerating dystrophic muscles

Project description:We report here on the identification and functional characterization of Sca1-positive muscle interstitial cells that contribute to regeneration or fibroadipogenic degeneration of dystrophic muscles and mediate the beneficial effects of HDAC inhibitors (HDACi) in mdx mice. We found that the phenotype adopted by these cells and their biological activity are influenced by changes in muscle environment. While Sca1-positive muscle interstitial cells from healthy muscles spontaneously adopt a fibro-adipogenic phenotype, Sca1-positive muscle interstitial cells isolated from dystrophic muscles of young mdx mice show a latent myogenic phenotype that is implemented by the exposure to HDACi. Co-culture assays in vitro and co-transplantation experiments in vivo demonstrate that HDACi also improve Sca1-positive muscle interstitial cell ability to enhance the differentiation potential of adjacent satellite cells. Importantly, HDACi-induced myogenic phenotype and pro-regeneration activity were not observed in Sca1-positive muscle interstitial cells isolated from muscles of old mdx mice. The different phenotype of Sca1-positive muscle interstitial cells from mdx mice at different stages of disease progression correlated with the stage-dependent beneficial effect of HDACi, which were effective only at early stages of disease. Transplantation of Sca1-positive muscle interstitial cells isolated from regenerating young muscles into muscles of old mdx mice restored HDACi ability to increase myofiber size. These results indicate that Sca1-positive muscle interstitial cells are key cellular determinants of disease progression and mediate the beneficial effect of HDACi in a mouse model of muscular dystrophy. Isolation of Sca1+ muscle interstitial cells from TSA treated DMD/MDX mice and MuSc from DMD/MDX mice

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Project description:Asynchronous skeletal muscle degeneration/regeneration is a hallmark feature of Duchenne muscular dystrophy (DMD); however, traditional -omics technologies that lack spatial context make it difficult to study the biological mechanisms of how asynchronous regeneration contributes to disease progression. Here, using the severely dystrophic D2-mdx mouse model, we generated a high-resolution cellular and molecular spatial atlas of dystrophic muscle by integrating spatial transcriptomics and single-cell RNAseq datasets.

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Dystrophic single myofibers vs. control single myofibers

Project description:MicroRNA-expression profile of dystrophic single fibers compared to wild type single fibers isolated from different muscles of mdx and C57BL mice. Myofibers were isolated from different muscle types (tibialis, diaphragm and quadriceps) of gender- (male) and age- (3 month old and half) matched wt and dystrophic mice. 9 total samples per animal model (C57BL, mdx), 3 replicates per muscle type.

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RNA-seq comparison of whole muscle between WT mice, dystrophic mice, and P2rx7-null dystrophic mice

Project description:Duchenne muscular dystrophy (DMD) is a debilitating and typically fatal X-linked progressive neuromuscular disorder that results in progressive muscle degeneration aggravated by sterile inflammation. The P2RX7 purinoceptor is an extracellular ATP-gated ion channel expressed in immune cells, and has been targeted in treatment of infectious and inflammatory diseases. In particular, P2xr7 receptor abnormalities have been demonstrated in mdx dystrophic mice, a model for DMD lacking expression of the full length dystrophin transcript through a single point mutation in exon 23. Here, we looked at the differential effects in gene expression regulation in whole muscle in dystrophic mdx mice with or without ablation of the P2rx7 purinoceptor.

2019-09-26 | E-MTAB-7698 | biostudies-arrayexpress

Dystrophic single myofibers vs. control single myofibers

Project description:MicroRNA-expression profile of dystrophic single fibers compared to wild type single fibers isolated from different muscles of mdx and C57BL mice.

2015-11-25 | GSE21498 | GEO

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