Cold shock protein RBM3 attenuates atrophy and induces hypertrophy in skeletal muscle.
Cold shock protein RBM3 attenuates atrophy and induces hypertrophy in skeletal muscle.
复制标题
冷休克蛋白 RBM3 可减轻骨骼肌萎缩并诱导骨骼肌肥大。
DOI:
10.1007/s10974-018-9496-x
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发表时间:
2018
影响因子:
2.7
通讯作者:
Dupont-Versteegden,EstherE
中科院分区:
文献类型:
--
作者:
VanPelt,DouglasW;Confides,AmyL;Judge,AndrewR;Vanderklish,PeterW;Dupont-Versteegden,EstherE
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. C2C12myotubes 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.