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Dystrophic single myofibers vs control single myofibers

ABSTRACT: MicroRNA-expression profile of dystrophic single fibres vs wild type single fibers isolated from different muscle of mdx and c57bl mice. Myofibers were isolated from different muscle type (tibialis, diaphragm and quadriceps of gender- (male) and age- (3 month old and half) matched wt and dystrophic mice).

ORGANISM(S): Mus musculus Rattus norvegicus synthetic construct Homo sapiens

PROVIDER: GSE21219 | GEO | 2012/12/21

SECONDARY ACCESSION(S): PRJNA126531

REPOSITORIES: GEO

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Dystrophic single myofibers vs control single myofibers

Project description:MicroRNA-expression profile of dystrophic single fibres vs wild type single fibers isolated from different muscle of mdx and c57bl mice. Myofibers were isolated from different muscle type (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, 3 replicates per muscle type sample

2012-12-21 | E-GEOD-21219 | 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. 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.

2015-11-25 | E-GEOD-21498 | 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

RNA-seq comparison of immortalised myoblasts from dystrophic and WT mice

Project description:Pathophysiology of Duchenne Muscular Dystrophy (DMD) is still elusive. Although progressive damage to muscle fibres is a cause of muscle deterioration leading to premature death, there is a growing body of evidence indicating that the triggering effects of DMD mutation are present at the very early stage of muscle development. To study this, we have performed an RNA-seq experiment to compare the transcriptional profile of early stage myoblasts from dystrophic mice compared to WT mice. We have used a myoblast cell line carrying the mdx mutant allele (SC5), which results in a premature stop codon in the Dystrophin gene, leading to a dystrophic phenotype. The WT cell line is the IMO myoblast cell line.

2019-10-02 | E-MTAB-7287 | biostudies-arrayexpress

Cells isolated from diaphragm of mdx mouse: satellite cells vs. PDGFRa+ cells

Project description:Transcriptional profiling of mouse skeletal muscle-derived cells comparing satellite cells with PDGFRa+ cells. Satellite cells and PDGFRa+ cells were directly isolated from diaphragm of dystrophic mdx mouse by FACS.

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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

effects of microbiome dysbiosis on murine dystrophic muscle

Project description:Duchenne muscular dystrophy (DMD) is a progressive severe muscle-wasting disease caused by mutations in DMD encoding dystrophin that leads to loss of muscle function with cardiac/respiratory failure and premature death. Since dystrophic muscles are sensed by infiltrating inflammatory cells and gut microbial communities can cause immune dysregulation and metabolic syndrome, we sought to investigate whether intestinal bacteria may support the muscle immune response in mdx dystrophic animal model. We assess this question here through unbiased profiling of muscle transcriptome through RNAseq. We found that the absence of gut microbes through the generation of a mdx GF animal model as well as modulation of the microbial community structure by antibiotic treatment revealed the ability of the dystrophic-associated intestinal microbiota to modulate immunity and secondary muscle pathogenetic mechanisms of DMD, including inflammation, fibrosis, and atrophy.

2022-11-22 | GSE218370 | GEO

Dystrophic single myofibers vs control single myofibers

Project description:Dystrophic single myofibers vs control single myofibers

| PRJNA126531 | ENA

Dystrophic single myofibers vs. control single myofibers

Project description:Dystrophic single myofibers vs. control single myofibers

| PRJNA125993 | ENA

Single Cell RNA-Sequencing of Skeletal Muscle in Dystrophic Mouse Models

Project description:Duchenne muscular dystrophy (DMD) is caused by an out-of-frame mutation in the DMD gene that results in the absence of a functional dystrophin protein, leading to a devastating and progressive lethal muscle-wasting disease. Genetic modifiers have been shown to increase disease severity in DMD mouse models as well as in human patients. Little is known about cellular heterogeneity in skeletal muscle as disease severity increases. To address this, we explored skeletal muscle-resident cell populations in healthy (wt-NSG), dystrophic (mdx-NSG), and severely dystrophic (mdxD2-NSG) mouse models utilizing scRNA-seq. We found an increased frequency of activated fibroblasts, activated fibro-adipogenic progenitor cells, and proinflammatory macrophages in dystrophic and severely dystrophic gastrocnemius muscles. Moreover, in endothelial cells we found an upregulation of extracellular matrix and platelet aggregation genes in dystrophic and severely dystrophic muscles, indicating endothelial cell functional impairment. In summary, this work extends the understanding of the severe nature of DMD, which should be considered when developing regenerative therapeutic avenues for DMD.

2022-09-27 | GSE213925 | GEO

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