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Cardiac muscle, comparisons of wild type and mdx mice, 8 week and 10.5 month (Porter lab)

ABSTRACT: Determination of gene expression changes in cardiac muscle of mdx (dystrophin-deficient) mice at postnatal ages 8 weeks and 10.5 months. 3 independent replicates/age/strain. Keywords: parallel sample

ORGANISM(S): Mus musculus

PROVIDER: GSE1471 | GEO | 2004/12/10

SECONDARY ACCESSION(S): PRJNA90055

REPOSITORIES: GEO

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Transcription profiling of mouse cardiac muscle from wild type and mdx mice, 8 week and 10.5 month (Porter lab)

Project description:Determination of gene expression changes in cardiac muscle of mdx (dystrophin-deficient) mice at postnatal ages 8 weeks and 10.5 months. 3 independent replicates/age/strain.

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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

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

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

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.

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

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