Title | Cold shock protein RBM3 attenuates atrophy and induces hypertrophy in skeletal muscle. |
Publication Type | Journal Article |
Year of Publication | 2018 |
Authors | Van Pelt DW, Confides AL, Judge AR, Vanderklish PW, Dupont-Versteegden EE |
Journal | J Muscle Res Cell Motil |
Volume | 39 |
Issue | 1-2 |
Pagination | 35-40 |
Date Published | 2018 04 |
ISSN | 1573-2657 |
Keywords | Animals, Cell Line, Cold Shock Proteins and Peptides, Dexamethasone, Hypertrophy, Male, Mice, Muscle Fibers, Skeletal, Muscular Atrophy, Rats, Rats, Inbred F344, RNA-Binding Proteins |
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. CC 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. |
DOI | 10.1007/s10974-018-9496-x |
Alternate Journal | J. Muscle Res. Cell. Motil. |
PubMed ID | 30051360 |
Grant List | R01NS066053 / NH / NIH HHS / United States |