Cold shock protein RBM3 attenuates atrophy and induces hypertrophy in skeletal muscle

Douglas W. Van Pelt, Amy L. Confides, Andrew R. Judge, Peter W. Vanderklish, Esther E. Dupont-Versteegden

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

RNA-binding motif protein 3 (RBM3), a stress-inducible RNA-binding protein that increases protein synthesis and confers cell protection in multiple cell types, has been identified as a possible regulator of skeletal muscle mass. Therefore, the primary aim of this study was to examine the impact of elevated RBM3 on skeletal muscle hypertrophy and resistance to atrophy. Plasmid-mediated overexpression of RBM3 in vitro and in vivo was used to assess the role of RBM3 in muscle. C2C12 myotubes overexpressing RBM3 were approximately 1.6 times larger than non-transfected myotubes, suggesting a role for RBM3 in hypertrophy. In addition, elevated RBM3 attenuated atrophy in myotubes exposed to dexamethasone. In agreement with in vitro results, overexpression of RBM3 in soleus muscle of F344/BN rats using electroporation techniques increased the cross sectional area of muscle fibers. Overexpression of RBM3 also attenuated muscle atrophy in rat soleus muscle undergoing disuse atrophy. These findings provide direct evidence for a novel role of RBM3 in inducing hypertrophy as well as attenuating atrophy.

Original languageEnglish
Pages (from-to)35-40
Number of pages6
JournalJournal of Muscle Research and Cell Motility
Volume39
Issue number1-2
DOIs
StatePublished - Apr 1 2018

Bibliographical note

Funding Information:
Acknowledgements This work was supported by NIH Grant AG028925 to ED-V, and NIH Grant R01NS066053 to PWV.

Publisher Copyright:
© 2018, Springer Nature Switzerland AG.

Keywords

  • RNA binding proteins
  • Skeletal muscle atrophy
  • Skeletal muscle hypertrophy
  • Translation

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Cell Biology

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