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

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

PROVIDER: PRJNA1023586 | ENA |

REPOSITORIES: ENA

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

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Effects of Pten knockout in dystrophic skeletal muscles of mdx mouse

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

2011-02-19 | GSE27129 | GEO

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

Dinoponera quadriceps

Project description:Dinoponera quadriceps overview

| PRJNA237674 | ENA

Myofiber branching rather than myofiber hyperplasia contributes to muscle hypertrophy in mdx mice.

Project description:Muscle hypertrophy in the mdx mouse model of Duchenne muscular dystrophy (DMD) can partially compensate for the loss of dystrophin by maintaining peak force production. Histopathology examination of the hypertrophic muscles suggests the hypertrophy primarily results from the addition of myofibers, and is accompanied by motor axon branching. However, it is unclear whether an increased number of innervated myofibers (myofiber hyperplasia) contribute to muscle hypertrophy in the mdx mice.To better understand the cellular mechanisms of muscle hypertrophy in mdx mice, we directly compared the temporal progression of the dystrophic pathology in the extensor digitorum longus (EDL) muscle to myofiber number, myofiber branching, and innervation, from 3 to 20 weeks of age.We found that a 28% increase in the number of fibers in transverse sections of muscle correlated with a 31% increase in myofiber branching. Notably, the largest increases in myofiber number and myofiber branching occurred after 12 weeks of age when the proportion of myofibers with central nuclei had stabilized and the mdx mouse had reached maturity. The dystrophic pathology coincided with profound changes to innervation of the muscles that included temporary denervation of necrotic fibers, fragmentation of synapses, and ultra-terminal axon sprouting. However, there was little evidence of synapse formation in the mdx mice from 3 to 20 weeks of age. Only 4.4% of neuromuscular junctions extended ultra-terminal synapses, which failed to mature, and the total number of neuromuscular junctions remained constant.Muscle hypertrophy in mdx mice results from myofiber branching rather than myofiber hyperplasia.

| S-EPMC4047439 | biostudies-literature

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