Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Age-related T2 changes in hindlimb muscles of mdx mice.

ABSTRACT: Magnetic resonance imaging (MRI) was used to monitor changes in the transverse relaxation time constant (T2) in lower hindlimb muscles of mdx mice at different ages.Young (5 weeks), adult (44 weeks), and old mdx (96 weeks), and age-matched control mice were studied. Young mdx mice were imaged longitudinally, whereas adult and old mdx mice were imaged at a single time-point.Mean muscle T2 and percent of pixels with elevated T2 were significantly different between mdx and control mice at all ages. In young mdx mice, mean muscle T2 peaked at 7-8 weeks and declined at 9-11 weeks. In old mdx mice, mean muscle T2 was decreased compared with young and adult mice, which could be attributed to fibrosis.MRI captured longitudinal changes in skeletal muscle integrity of mdx mice. This information will be valuable for pre-clinical testing of potential therapeutic interventions for muscular dystrophy.

SUBMITTER: Vohra RS

PROVIDER: S-EPMC4600631 | biostudies-literature | 2016 Jan

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

Age-related T2 changes in hindlimb muscles of mdx mice.

Vohra Ravneet S RS Mathur Sunita S Bryant Nathan D ND Forbes Sean C SC Vandenborne Krista K Walter Glenn A GA

Muscle & nerve 20150714 1

<h4>Introduction</h4>Magnetic resonance imaging (MRI) was used to monitor changes in the transverse relaxation time constant (T2) in lower hindlimb muscles of mdx mice at different ages.<h4>Methods</h4>Young (5 weeks), adult (44 weeks), and old mdx (96 weeks), and age-matched control mice were studied. Young mdx mice were imaged longitudinally, whereas adult and old mdx mice were imaged at a single time-point.<h4>Results</h4>Mean muscle T2 and percent of pixels with elevated T2 were significantl ...[more]

PMID: 25846867

Similar Datasets

Extraocular, hindlimb, and cardiac muscles, comparison of dko and mdx mice (Porter lab)

Project description:Comparison by expression profiling of tissue from dKO (utrophin/dystrophin-deficient) and MDX mice at 8 weeks of age. Independent triplicate analyses/strain were done for extraocular, hindlimb, and cardiac muscle. Keywords = microarray Keywords = extraocular Keywords: parallel sample

2004-12-08 | GSE1463 | GEO

Transcription profiling of extraocular, hindlimb and cardiac muscles from dKO and MDX mice

2007-12-04 | E-GEOD-1463 | biostudies-arrayexpress

Hormonal receptors in skeletal muscles of dystrophic mdx mice.

Project description:INTRODUCTION: Several evidences show that muscles have an endocrine function. Glucocorticoid, estrogen, progesterone, and testosterone receptors have already been found in normal skeletal muscles, but not in dystrophic muscles. METHODS: The gene expression of hormone receptors was compared between dystrophic and healthy muscles in mdx and C57BL6 mice strains. RESULTS: The mdx mice showed a significant increase in the steroid receptors mRNA when compared to the C57BL6 mice: levels of androgen(s) receptors in the heart, estrogen receptors alpha in the EDL, and estrogen receptors beta in the quadriceps were increased. In addition, significant lowered levels of some other hormone receptors were found: corticosteroid receptors in the EDL and estrogen receptors alpha in the quadriceps. CONCLUSION: Dystrophic muscles bear significant differences in the expression of hormone receptors when compared to the C57BL6 mice strain. The importance of such differences is yet to be better understood.

| S-EPMC3591173 | biostudies-literature

Treatment of Dystrophic mdx Mice with an ADAMTS-5 Specific Monoclonal Antibody Increases the Ex Vivo Strength of Isolated Fast Twitch Hindlimb Muscles.

Project description:Aberrant extracellular matrix synthesis and remodeling contributes to muscle degeneration and weakness in Duchenne muscular dystrophy (DMD). ADAMTS-5, a secreted metalloproteinase with catalytic activity against versican, is implicated in myogenesis and inflammation. Here, using the mdx mouse model of DMD, we report increased ADAMTS-5 expression in dystrophic hindlimb muscles, localized to regions of regeneration and inflammation. To investigate the pathophysiological significance of this, 4-week-old mdx mice were treated with an ADAMTS-5 monoclonal antibody (mAb) or IgG2c (IgG) isotype control for 3 weeks. ADAMTS-5 mAb treatment did not reduce versican processing, as protein levels of the cleaved versikine fragment did not differ between hindlimb muscles from ADAMTS-5 mAb or IgG treated mdx mice. Nonetheless, ADAMTS-5 blockade improved ex vivo strength of isolated fast extensor digitorum longus, but not slow soleus, muscles. The underpinning mechanism may include modulation of regenerative myogenesis, as ADAMTS-5 blockade reduced the number of recently repaired desmin positive myofibers without affecting the number of desmin positive muscle progenitor cells. Treatment with the ADAMTS-5 mAb did not significantly affect makers of muscle damage, inflammation, nor fiber size. Altogether, the positive effects of ADAMTS-5 blockade in dystrophic muscles are fiber-type-specific and independent of versican processing.

| S-EPMC7175239 | biostudies-literature

A multigene analysis of the effects of L-arginine treatment in the hindlimb and diaphragm muscles of mdx mice.

Project description:Diaphragm and hindlimb muscle samples from BL10 or MDX mice treated with L-arginine or untreated. Ages 3/5/9/12 weeks are represented in analysis. Keywords = Muscular dystrophy Keywords = mdx Keywords = DNA microarrays Keywords = L-arginine Keywords = gene expression profiling Keywords: other

2004-08-10 | GSE1636 | GEO

A multigene analysis of the effects of L-arginine treatment in the hindlimb and diaphragm muscles of mdx mice.

2004-08-10 | E-GEOD-1636 | biostudies-arrayexpress

Poloxamer 188 reduces the contraction-induced force decline in lumbrical muscles from mdx mice.

Project description:Duchenne Muscular Dystrophy is a genetic disease caused by the lack of the protein dystrophin. Dystrophic muscles are highly susceptible to contraction-induced injury, and following contractile activity, have disrupted plasma membranes that allow leakage of calcium ions into muscle fibers. Because of the direct relationship between increased intracellular calcium concentration and muscle dysfunction, therapeutic outcomes may be achieved through the identification and restriction of calcium influx pathways. Our purpose was to determine the contribution of sarcolemmal lesions to the force deficits caused by contraction-induced injury in dystrophic skeletal muscles. Using isolated lumbrical muscles from dystrophic (mdx) mice, we demonstrate for the first time that poloxamer 188 (P188), a membrane-sealing poloxamer, is effective in reducing the force deficit in a whole mdx skeletal muscle. A reduction in force deficit was also observed in mdx muscles that were exposed to a calcium-free environment. These results, coupled with previous observations of calcium entry into mdx muscle fibers during a similar contraction protocol, support the interpretation that extracellular calcium enters through sarcolemmal lesions and contributes to the force deficit observed in mdx muscles. The results provide a basis for potential therapeutic strategies directed at membrane stabilization of dystrophin-deficient skeletal muscle fibers.

| S-EPMC2493563 | biostudies-literature

Comparison of age-related changes in gene expression of 2 rat skeletal muscles

Project description:In this study we compared Gastrocnemius and Triceps gene expression with age. Our results show that gene expression is massively modulated with age in Gastroc but on the contrary very stable in Triceps, suggesting that Triceps is resistant to age-related defects. 3 groups of age (8 months, 18 months and 24 months) were analyzed, with 9-10 replicates per group. Gastrocnemius and Triceps were collected for each animal.

2016-05-12 | E-GEOD-78702 | biostudies-arrayexpress

Comparison of age-related changes in gene expression of 2 rat skeletal muscles

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

2020-03-14 | GSE146977 | GEO

Sustained dystrophin expression induced by peptide-conjugated morpholino oligomers in the muscles of mdx mice.

Project description:Cell-penetrating peptides (CPPs), containing arginine (R), 6-aminohexanoic acid (X), and/or beta-alanine (B) conjugated to phosphorodiamidate morpholino oligomers (PMOs), enhance their delivery in cell culture. In this study, the potency, functional biodistribution, and toxicity of these conjugates were evaluated in vivo, in EGFP-654 transgenic mice that ubiquitously express the aberrantly spliced EGFP-654 pre-mRNA reporter. Correct splicing and enhanced green fluorescence protein (EGFP) upregulation serve as a positive readout for peptide-PMO (PPMO) entry into cells and access to EGFP-654 pre-mRNA in the nucleus. Intraperitoneal injections of a series of PPMOs, A-N (12 mg/kg), administered once a day for four successive days resulted in splicing correction in numerous tissues. PPMO-B was highly potent in the heart, diaphragm, and quadriceps, which are key muscles in the treatment of Duchenne muscular dystrophy. We therefore investigated PPMO M23D-B, designed to force skipping of stop-codon containing dystrophin exon 23, in an mdx mouse model of the disease. Systemic delivery of M23D-B yielded persistent exon 23 skipping, yielding high and sustained dystrophin protein expression in body-wide muscles, including cardiac muscle, without detectable toxicity. The rescued dystrophin reduced serum creatinine kinase to near-wild-type levels, indicating improvement in muscle integrity. This is the first report of oligonucleotide-mediated exon skipping and dystrophin protein induction in the heart of treated animals.

| S-EPMC2671676 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data