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Genome-wide expression analysis comparing hypertrophic changes in normal and dysferlinopathy mice.

Lee YS, Talbot CC, Lee SJ - Genom Data (2015)

Bottom Line: Because myostatin normally limits skeletal muscle growth, there are extensive efforts to develop myostatin inhibitors for clinical use.Hence, benefits of this approach should be weighed against these potential detrimental effects.Here, we present detailed experimental methods and analysis for the gene expression profiling described in our recently published study in Human Molecular Genetics (Lee et al., 2015).

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, 725 North Wolfe Street, PCTB 803, Baltimore, MD 21205, USA.

ABSTRACT
Because myostatin normally limits skeletal muscle growth, there are extensive efforts to develop myostatin inhibitors for clinical use. One potential concern is that in muscle degenerative diseases, inducing hypertrophy may increase stress on dystrophic fibers. Our study shows that blocking this pathway in dysferlin deficient mice results in early improvement in histopathology but ultimately accelerates muscle degeneration. Hence, benefits of this approach should be weighed against these potential detrimental effects. Here, we present detailed experimental methods and analysis for the gene expression profiling described in our recently published study in Human Molecular Genetics (Lee et al., 2015). Our data sets have been deposited in the Gene Expression Omnibus (GEO) database (GSE62945) and are available at http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE62945. Our data provide a resource for exploring molecular mechanisms that are related to hypertrophy-induced, accelerated muscular degeneration in dysferlinopathy.

No MeSH data available.


Related in: MedlinePlus

Microarray quality assessment of 18 chips for three biological replicates in 6 different groups; wt, Dysf−/−, F66, F66;Dysf−/−, and ACVR2B/Fc-injected wt and Dysf−/− mice. (a) Box plots of 18 chips show median-centered raw data distributions. (b) Line graphs of 18 chips also support that all the chips' probes have signals of similar distribution and median value. (c) The magnitude of between class variation (myostatin inhibition by ACVR2B/Fc and F66, and dysferlin deficiency) is compared to that of within-class variation (Error), demonstrating biological variation to be far greater than experimental noise.
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f0005: Microarray quality assessment of 18 chips for three biological replicates in 6 different groups; wt, Dysf−/−, F66, F66;Dysf−/−, and ACVR2B/Fc-injected wt and Dysf−/− mice. (a) Box plots of 18 chips show median-centered raw data distributions. (b) Line graphs of 18 chips also support that all the chips' probes have signals of similar distribution and median value. (c) The magnitude of between class variation (myostatin inhibition by ACVR2B/Fc and F66, and dysferlin deficiency) is compared to that of within-class variation (Error), demonstrating biological variation to be far greater than experimental noise.

Mentions: Affymetrix CEL files generated by GeneChip Command Console software were extracted and normalized using the Robust Multichip Analysis (RMA) algorithm in Partek Genomics Suite v6.6 software (Partek Inc., St. Louis, USA) [5]. To ensure exploration of the broadest range of gene transcripts, we imported all 641,130 Affymetrix “Extended Meta-probesets”. Quality control assessments were run (Fig. 1) and these exon-level probesets were summarized into 115,830 transcripts, of which 34,343 currently had annotation at the gene level. As the understanding of genomics and information on the mouse genome increase these values will change over time, with the June 2015 annotation showing 47,252 gene-level transcripts.


Genome-wide expression analysis comparing hypertrophic changes in normal and dysferlinopathy mice.

Lee YS, Talbot CC, Lee SJ - Genom Data (2015)

Microarray quality assessment of 18 chips for three biological replicates in 6 different groups; wt, Dysf−/−, F66, F66;Dysf−/−, and ACVR2B/Fc-injected wt and Dysf−/− mice. (a) Box plots of 18 chips show median-centered raw data distributions. (b) Line graphs of 18 chips also support that all the chips' probes have signals of similar distribution and median value. (c) The magnitude of between class variation (myostatin inhibition by ACVR2B/Fc and F66, and dysferlin deficiency) is compared to that of within-class variation (Error), demonstrating biological variation to be far greater than experimental noise.
© Copyright Policy - CC BY-NC-ND
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4664771&req=5

f0005: Microarray quality assessment of 18 chips for three biological replicates in 6 different groups; wt, Dysf−/−, F66, F66;Dysf−/−, and ACVR2B/Fc-injected wt and Dysf−/− mice. (a) Box plots of 18 chips show median-centered raw data distributions. (b) Line graphs of 18 chips also support that all the chips' probes have signals of similar distribution and median value. (c) The magnitude of between class variation (myostatin inhibition by ACVR2B/Fc and F66, and dysferlin deficiency) is compared to that of within-class variation (Error), demonstrating biological variation to be far greater than experimental noise.
Mentions: Affymetrix CEL files generated by GeneChip Command Console software were extracted and normalized using the Robust Multichip Analysis (RMA) algorithm in Partek Genomics Suite v6.6 software (Partek Inc., St. Louis, USA) [5]. To ensure exploration of the broadest range of gene transcripts, we imported all 641,130 Affymetrix “Extended Meta-probesets”. Quality control assessments were run (Fig. 1) and these exon-level probesets were summarized into 115,830 transcripts, of which 34,343 currently had annotation at the gene level. As the understanding of genomics and information on the mouse genome increase these values will change over time, with the June 2015 annotation showing 47,252 gene-level transcripts.

Bottom Line: Because myostatin normally limits skeletal muscle growth, there are extensive efforts to develop myostatin inhibitors for clinical use.Hence, benefits of this approach should be weighed against these potential detrimental effects.Here, we present detailed experimental methods and analysis for the gene expression profiling described in our recently published study in Human Molecular Genetics (Lee et al., 2015).

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, 725 North Wolfe Street, PCTB 803, Baltimore, MD 21205, USA.

ABSTRACT
Because myostatin normally limits skeletal muscle growth, there are extensive efforts to develop myostatin inhibitors for clinical use. One potential concern is that in muscle degenerative diseases, inducing hypertrophy may increase stress on dystrophic fibers. Our study shows that blocking this pathway in dysferlin deficient mice results in early improvement in histopathology but ultimately accelerates muscle degeneration. Hence, benefits of this approach should be weighed against these potential detrimental effects. Here, we present detailed experimental methods and analysis for the gene expression profiling described in our recently published study in Human Molecular Genetics (Lee et al., 2015). Our data sets have been deposited in the Gene Expression Omnibus (GEO) database (GSE62945) and are available at http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE62945. Our data provide a resource for exploring molecular mechanisms that are related to hypertrophy-induced, accelerated muscular degeneration in dysferlinopathy.

No MeSH data available.


Related in: MedlinePlus