title: Genome-wide expression analysis comparing hypertrophic changes in normal and dysferlinopathy mice.
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.
authors.affiliation: Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, 725 North Wolfe Street, PCTB 803, Baltimore, MD 21205, USA.
authors.forename: Yun-Sil
authors.initials: YS
authors.lastname: Lee
authors.affiliation: Institute for Basic Biomedical Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
authors.forename: C Conover
authors.initials: CC
authors.lastname: Talbot
authors.affiliation: Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, 725 North Wolfe Street, PCTB 803, Baltimore, MD 21205, USA.
authors.forename: Se-Jin
authors.initials: SJ
authors.lastname: Lee
keywords: ACVR2B/Fc; Dysferlinopathy; Follistatin; Myostatin; Skeletal muscle