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

Yun Sil Lee, C. Conover Talbot, Se Jin Lee

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish (US)
Pages (from-to)253-257
Number of pages5
JournalGenomics Data
Volume6
DOIs
StatePublished - Dec 1 2015

Keywords

  • ACVR2B/Fc
  • Dysferlinopathy
  • Follistatin
  • Myostatin
  • Skeletal muscle

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Medicine
  • Genetics

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