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
复制
发表时间:
2018
影响因子:
2.7
通讯作者:
Dupont-Versteegden,EstherE
Dupont-Versteegden,EstherE
中科院分区:
生物学3区
文献类型:
--
作者:
VanPelt,DouglasW;Confides,AmyL;Judge,AndrewR;Vanderklish,PeterW;Dupont-Versteegden,EstherE

文献摘要

相似文献

RNA结合基序蛋白3(RBM3)是一种应激诱导的RNA结合蛋白,可增加蛋白质合成并在多种细胞类型中提供细胞保护,已被确定为可能的骨骼肌质量调节因子。因此,这项研究的主要目的是研究RBM3升高对骨骼肌肥大和抗萎缩的影响。采用体外和体内表达载体的方法检测RBM3在肌肉组织中的表达。过表达RBM3的C2C12肌管约为未转染肌管的1.6倍,提示RBM3在肥大中起一定作用。此外,升高的RBM3可减轻地塞米松引起的肌管萎缩。利用电穿孔技术在F344/BN大鼠比目鱼肌中过表达RBM3的结果与体外结果一致,增加了肌肉纤维的横截面积。RBM3的过表达也减轻了经历废用性萎缩的大鼠比目鱼肌的肌肉萎缩。这些发现为RBM3在诱导肥大和减轻萎缩中的新作用提供了直接证据。
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.