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E-GEOD-1025

ABSTRACT: Transcription profiling of mouse hindlimb muscle, comparison of wild type and mdx mice, 7 to 112 Day

OTHER RELATED OMICS DATASETS IN: PRJNA87063PRJNA87093

PROVIDER: E-GEOD-1025 | ExpressionAtlas | 2014-08-14

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-1025-analysis-methods.tsv	Tabular
	E-GEOD-1025-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-1025-configuration.xml	Xml
	E-GEOD-1025-percentile-ranks.tsv	Tabular
	E-GEOD-1025.condensed-sdrf.tsv	Tabular

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Mus musculus

Project description:Hindlimb muscle, comparison of wild type and mdx mice, 7 to 112 Day (Porter lab)

| PRJNA87093 | ENA

Transcriptomics of heart and muscle tissues of transgenic or mdx mice (DMD disease model) with UAA incorporation systems

Project description:We constructed the trans/mdx mice as a novel DMD disease model by crossing transgenic mice and mdx mice. The transgenic and trans/mdx mice have UAA incorporation system that can readthrough the nonsense mutation in the dmd gene with additional UAA. The whole transcriptomics of heart and muscle tissues of 5 mouse groups (n=2) were used to determine whether the introduced UAA incorporation system affect the normal gene expression of mice, or the safety of the system. Groups include: a) wild-type C57BL/6N mice; b) transgenic mice; c) mdx mice; d) trans/mdx mice without UAA; e) trans/mdx mice with UAA (50 mg NAEK every 2-3 day, treated for 4 weeks). The total numbers of expressed genes were around 11,000 in all 5 mouse groups. The expression levels of major genes (logFPKM>0) in 5 mouse groups were also close to each other. These data indicated that the UAA incorporation system was safe and could serve as a potential therapeutic strategy for DMD disease. The transgenic mice with UAA incorporation system we constructed could also cross with other nonsense mutation mice to build more functional animal models.

2020-10-03 | GSE158961 | GEO

Blastocyst Injection of Wild Type Embryonic Stem Cells Induces Global Corrections in Mdx Mice.

2008-08-30 | GSE12580 | GEO

Jarrah2014 - mathematical model of the immune response in muscle degeneration and subsequent regeneration in Duchenne muscular dystrophy in mdx mice

Project description:Duchenne muscular dystrophy (DMD) is a genetic disease that results in the death of affected boys by early adulthood.The genetic defect responsible for DMD has been known for over 25 years, yet at present there is neither cure nor effective treatment for DMD. During early disease onset, the mdx mouse has been validated as an animal model for DMD and use of this model has led to valuable but incomplete insights into the disease process. For example, immune cells are thought to be responsible for a significant portion of muscle cell death in the mdx mouse; however, the role and time course of the immune response in the dystrophic process have not been well described. In this paper we constructed a simple mathematical model to investigate the role of the immune response in muscle degeneration and subsequent regeneration in the mdx mouse model of Duchenne muscular dystrophy. Our model suggests that the immune response contributes substantially to the muscle degeneration and regeneration processes. Furthermore, the analysis of the model predicts that the immune system response oscillates throughout the life of the mice, and the damaged fibers are never completely cleared.

2024-09-02 | BIOMD0000001015 | BioModels

Compare gene expression patterns in Chsy-1 wt and ko mouse 13.5 days embryo forelimbs

Project description:Transcriptional profiling of 13.5 day mouse embryo forelimbs. Gene expression comparison done between wild type and Chsy-1 gene knockout mice.

2014-06-01 | GSE29694 | GEO

Multi-level omics analysis of dystrophin loss and therapeutic restoration in a murine model [microRNA]

Project description:Duchenne muscular dystrophy (DMD) is a classical monogenic disorder, a model disease for genomic studies and a priority candidate for regenerative medicine and gene therapy. Although the genetic cause of DMD is well known, the molecular pathogenesis of disease and the response to therapy are incompletely understood. Here, we describe analyses of protein, mRNA and microRNA expression in the tibialis anterior of the mdx mouse model of DMD. Notably, 3272 proteins were quantifiable and 525 identified as differentially expressed in mdx muscle (P < 0.01). Therapeutic restoration of dystrophin by exon skipping induced widespread shifts in protein and mRNA expression towards wild-type expression levels, whereas the miRNome was largely unaffected. Comparison analyses between datasets showed that protein and mRNA ratios were only weakly correlated (r = 0.405), and identified a multitude of differentially affected cellular pathways, upstream regulators and predicted miRNA–target interactions. This study provides fundamental new insights into gene expression and regulation in dystrophic muscle. 3 Wt, 4 mdx and 4 Pip6e-PMO treated mdx mice

2015-09-24 | E-GEOD-64419 | biostudies-arrayexpress

Multi-level omics analysis of gene expression in a murine model of dystrophin loss and therapeutic restoration [mRNA]

Project description:Duchenne muscular dystrophy (DMD) is a classical monogenic disorder, a model disease for genomic studies and a priority candidate for regenerative medicine and gene therapy. Although the genetic cause of DMD is well known, the molecular pathogenesis of disease and the response to therapy are incompletely understood. Here,we describe analyses of protein, mRNA and microRNA expression in the tibialis anterior of the mdx mouse model of DMD. Notably, 3272 proteins were quantifiable and 525 identified as differentially expressed in mdx muscle (P < 0.01). Therapeutic restoration of dystrophin by exon skipping induced widespread shifts in protein and mRNA expression towards wild-type expression levels, whereas the miRNome was largely unaffected. Comparison analyses between datasets showed that protein and mRNA ratios were only weakly correlated (r = 0.405), and identified a multitude of differentially affected cellular pathways, upstream regulators and predicted miRNA–target interactions. This study provides fundamental new insights into gene expression and regulation in dystrophic muscle. 3 Wt, 4 mdx and 4 Pip6e-PMO treated mdx mice

2015-09-24 | E-GEOD-64418 | biostudies-arrayexpress

Fibro-adipogenic progenitors of dystrophic mice are insensitive to NOTCH regulation of adipogenesis

Project description:Fibro adipogenic progenitors (FAPs) promote satellite cell differentiation in adult skeletal muscle regeneration. However, in pathological conditions, FAPs are responsible for fibrosis and fatty infiltrations. Here we show that the NOTCH pathway negatively modulates FAP differentiation both in vitro and in vivo. However, FAPs isolated from young dystrophin- deficient mdx mice are insensitive to this control mechanism. An unbiased mass spectrometry-based proteomic analysis of FAPs from muscles of wild type and mdx mice, suggest that the synergistic cooperation between NOTCH and inflammatory signals controls FAP differentiation. Remarkably, we demonstrated that factors released by hematopoietic cells restore the sensitivity to NOTCH adipogenic inhibition in mdx FAPs. These results offer a basis for rationalizing pathological ectopic fat infiltrations in skeletal muscle and may suggest new therapeutic strategies to mitigate the detrimental effects of fat depositions in muscles of dystrophic patients.

2019-06-24 | PXD014195 | Pride

Transcription profiling of mouse wild type embryonic stem cells after blastocytst injection revealglobal corrections in MDX mice.

Project description:Duchenne muscular dystrophy (DMD) is an incurable neuromuscular degenerative disease, caused by a mutation in the dystrophin gene. Mdx mice recapitulate DMD features. Here we show that injection of wild-type (WT) embryonic stem cells (ESCs) into mdx blastocysts produces mice with improved pathology. A small fraction of WT ESCs incorporates into the mdx mouse nonuniformly to upregulate protein levels of dystrophin in the skeletal muscle. The chimeric muscle shows reduced regeneration and restores dystrobrevin, a dystrophin-related protein, in areas with high and with low dystrophin content. WT ESC injection also normalizes the amount of fat, a tissue that does not express dystrophin. ESC injection without dystrophin does not prevent the appearance of phenotypes in the skeletal muscle or in the fat. Thus, dystrophin supplied by the ESCs reverses disease in mdx mice globally. Experiment Overall Design: 3-week old mdx (C57BL/10ScSn-Dmdmdx/J, Jax labs) females were superovulated and mated with mdx males (Jax labs). Blastocysts were collected at 3.5 days afer mating, injected with 15 WT or mdx R26 ES cells. Injected blastocysts were then transferred into the uteri of pseudopregnant females and allowed to develop to term. Skeletal muscle from 4 month old chimeric male mice was collected, RNA was isolated and microarray analysis were performed.

2008-10-25 | E-GEOD-12580 | biostudies-arrayexpress

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).

2012-12-21 | GSE21219 | GEO

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