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Long noncoding RNA SMUL suppresses SMURF2 production-mediated muscle atrophy via nonsense-mediated mRNA decay

文献类型： 外文期刊

作者： Cai, Bolin 1 ; Li, Zhenhui 1 ; Ma, Manting 1 ; Zhang, Jing 1 ; Kong, Shaofen 1 ; Abdalla, Bahareldin Ali 1 ; Xu, Haipi 1 ;

作者机构： 1.South China Agr Univ, Coll Anim Sci, Lingnan Guangdong Lab Modern Agr, Guangzhou 510642, Guangdong, Peoples R China

2.South China Agr Univ, State Key Lab Conservat & Utilizat Subtrop Agrobi, Guangzhou 510642, Guangdong, Peoples R China

3.Jackson Lab, 600 Main St, Bar Harbor, ME 04609 USA

4.Rockefeller Univ, Lab Neurobiol & Behav, New York, NY 10065 USA

5.Minist Agr, Guangdong Prov Key Lab Agroanim Genom & Mol Breed, Guangzhou 510642, Guangdong, Peoples R China

6.Minist Agr, Key Lab Chicken Genet Breeding & Reprod, Guangzhou 510642, Guangdong, Peoples R China

期刊名称：MOLECULAR THERAPY-NUCLEIC ACIDS （ 影响因子：7.032； 五年影响因子：6.814 ）

ISSN： 2162-2531

年卷期： 2021 年 23 卷

页码：

收录情况： SCI

摘要： As the world population grows, muscle atrophy leading to muscle wasting could become a bigger risk. Long noncoding RNAs (lncRNAs) are known to play important roles in muscle growth and muscle atrophy. Meanwhile, it has recently come to light that many putative small open reading frames (sORFs) are hidden in lncRNAs; however, their translational capabilities and functions remain unclear. In this study, we uncovered 104 myogenic-associated lncRNAs translated, in at least a small peptide, by integrated transcriptome and proteomic analyses. Furthermore, an upstream ORF (uORF) regulatory network was constructed, and a novel muscle atrophy-associated lncRNA named SMUL (Smad ubiquitin regulatory factor 2 [SMURF2] upstream lncRNA) was identified. SMUL was highly expressed in skeletal muscle, and its expression level was down regulated during myoblast differentiation. SMUL promoted myoblast proliferation and suppressed differentiation in vitro. In vivo, SMUL induced skeletal muscle atrophy and promoted a switch from slow-twitch to fast-twitch fibers. In the meantime, translation of the SMUL sORF disrupted the stability of SMURF2 mRNA. Mechanistically, SMUL restrained SMURF2 production via nonsense-mediated mRNA decay (NMD), participating in the regulation of the transforming growth factor beta (TGF-beta)/SMAD pathway and further regulating myogenesis and muscle atrophy. Taken together, these results suggest that SMUL could be a novel therapeutic target for muscle atrophy.

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