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Gene expression profiles using microarrays in mdx and mdx/MMP-2-/- mice at 1 and 3 months of age

ABSTRACT: Matrix metalloprotease (MMP) -2 has been reported to be up-regulated in skeletal muscle in the lethal X-linked muscle disorder Duchenne muscular dystrophy (DMD), which is caused by loss of dystrophin. However, the role of MMP-2 in dystrophin-deficient muscle is not well known. The aim of this study was to verify the role of MMP-2 in dystrophin-deficient muscle by using mdx mice with genetic ablation of MMP-2 (mdx/MMP-2-/-). Gene expression profiles were analyzed in the skeletal muscle of mdx and mdx/MMP-2-/- mice at 1 and 3 months of age.

ORGANISM(S): Mus musculus

PROVIDER: GSE27129 | GEO | 2011/02/19

SECONDARY ACCESSION(S): PRJNA137421

REPOSITORIES: GEO

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Gene expression profiles using microarrays in mdx and mdx/MMP-2-/- mice at 1 and 3 months of age

Project description:Matrix metalloprotease (MMP) -2 has been reported to be up-regulated in skeletal muscle in the lethal X-linked muscle disorder Duchenne muscular dystrophy (DMD), which is caused by loss of dystrophin. However, the role of MMP-2 in dystrophin-deficient muscle is not well known. The aim of this study was to verify the role of MMP-2 in dystrophin-deficient muscle by using mdx mice with genetic ablation of MMP-2 (mdx/MMP-2-/-). Gene expression profiles were analyzed in the skeletal muscle of mdx and mdx/MMP-2-/- mice at 1 and 3 months of age. Tibialis anterior muscle was isolated from four groups of mice (mdx and mdx/MMP-2-/- mice at 1 and 3 months of age). Total RNA was purified and prepared for hybridization to Affymetrix Mouse Genome 430 2.0 arrays (Affymetrix Inc., Santa Clara, CA, USA) using Affymetrix reagents and protocols. The mRNA levels of differentially expressed genes from gene chip analysis were confirmed by quantitative real-time PCR assay.

2011-02-19 | E-GEOD-27129 | biostudies-arrayexpress

iTRAQ Protemics of mdx vs. mdx/Actg1-TG mouse skeletal muscle

Project description:Duchenne muscular dystrophy (DMD) is an X-linked recessive disease caused by deleterious mutations in the DMD gene, rendering non-functional forms or complete absence of the protein dystrophin. Eccentric contraction-induced force loss is the most robust and reproducible phenotype of dystrophin-deficient skeletal muscle, yet the molecular mechanisms underlying force loss remain obscure. To this end, we utilized the mdx mouse model of DMD, which displays extreme sensitivity to eccentric contractions. An existing mouse line from our lab that overexpresses cytoplasmic gamma-actin specifically in skeletal muscle (mdx/Actg1-TG) was shown to significantly protect mdx muscle against contraction-induced force loss. To understand the mechanism behind this protection, we performed iTRAQ proteomics on mdx/Actg1-TG tibialis anterior (TA) muscle versus non-transgenic littermate controls to identify differentially-expressed proteins that may afford protection upon gamma-actin overexpression.

2018-10-22 | PXD009680 | Pride

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 [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

mRNA expression in regenerated mdx mouse skeletal muscle

Project description:Despite over 3,000 articles published on dystrophin in the last 15 years, the reasons underlying the progression of the human disease, differential muscle involvement, and disparate phenotypes in different species are not understood. The present experiment employed a screen of 12,488 mRNAs in 16-wk-old mouse mdx muscle at a time when the skeletal muscle is avoiding severe dystrophic pathophysiology, despite the absence of a functional dystrophin protein. A number of transcripts whose levels differed between the mdx and human Duchenne muscular dystrophy were noted. A fourfold decrease in myostatin mRNA in the mdx muscle was noted. Differential upregulation of actin-related protein 2/3 (subunit 4), beta-thymosin, calponin, mast cell chymase, and guanidinoacetate methyltransferase mRNA in the more benign mdx was also observed. Transcripts for oxidative and glycolytic enzymes in mdx muscle were not downregulated. These discrepancies could provide candidates for salvage pathways that maintain skeletal muscle integrity in the absence of a functional dystrophin protein in mdx skeletal muscle. Keywords: other

2003-07-16 | GSE466 | GEO

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

2008-08-30 | GSE12580 | GEO

Transcription profiling of 16-week-old mdx mouse muscles to characterize transcriptional changes induced by dystrophin deficiency.

2007-11-06 | E-GEOD-466 | biostudies-arrayexpress

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

Expression data from quadriceps of myofiber mineralocorticoid receptor conditional knockout (MRcko)/mdx and myeloid cell MRcko/mdx mice compared to Cre-/mdx control mice

Project description:To identify the gene expression differences in skeletal muscles resulting from conditional knockout of the mineralocorticoid receptor in myofibers and myeloid cells in dystrophin-deficient mdx mice

2024-04-03 | GSE244569 | GEO

miR-206 modulates the pathogenesis of muscular dystrophy of mdx mice

Project description:In response to skeletal muscle injury, adult myogenic stem cells, known as satellite cells, are activated and undergo proliferation and differentiation to regenerate new muscle fibers. The skeletal muscle-specific microRNA, miR-206, is up-regulated in satellite cells following muscle injury, but its role in muscle regeneration has not been defined. Here we show that skeletal muscle regeneration in response to cardiotoxin injury is impaired in mice lacking miR-206. Loss of miR-206 also accelerates and exacerbates the dystrophic phenotype of mdx mice, a model for Duchenne muscular dystrophy. MiR-206 promotes satellite cell differentiation and fusion to form multinucleated myofibers by suppressing a collection of negative regulators of myogenesis. Our findings reveal an essential role for miR-206 in satellite cell differentiation during skeletal muscle regeneration and as a modulator of Duchenne muscular dystrophy. total RNA obtained from TA muscle of mdx and 3 miR-206 KO; mdx mice at 3 months of age.

2012-04-30 | E-GEOD-36077 | biostudies-arrayexpress

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