Lnc-mg is a long non-coding RNA that promotes myogenesis.
Lnc-mg is a long non-coding RNA that promotes myogenesis.
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Lnc-mg是一种长链非编码RNA，可促进肌生成
DOI：
10.1038/ncomms14718
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发表时间：
2017-03-10
影响因子：
16.6
通讯作者：
Wang X
中科院分区：
文献类型：
--
作者：
Zhu M;Liu J;Xiao J;Yang L;Cai M;Shen H;Chen X;Ma Y;Hu S;Wang Z;Hong A;Li Y;Sun Y;Wang X
最近的研究表明，长链非编码rna （lncRNAs）在肌肉发生和成人骨骼肌再生中起着重要的调节作用。然而，lncrna在成体骨骼肌干细胞的成肌分化和成肌过程中的具体作用在很大程度上仍然未知。在这里，我们确定了一个在骨骼肌中特异性富集的lncRNA（肌生成相关lncRNA，简称lnc-mg）。在小鼠中，骨骼肌中lnc-mg的条件敲除会导致肌肉萎缩和运动时肌肉耐力的丧失。另外，骨骼肌特异性过表达lnc-mg会促进肌肉肥大。对原代骨骼肌细胞的体外分析表明，lnc-mg在成肌分化过程中逐渐增加，其过表达促进细胞分化。在机制上，lnc-mg通过作为microRNA-125b的竞争内源性RNA （ceRNA）来控制胰岛素样生长因子2的蛋白丰度，从而促进肌肉的发生。这些发现表明lnc-mg是肌肉细胞分化和骨骼肌发育的一种新的非编码调节因子。长链非编码mrna在肌肉发育和再生中发挥重要作用。在这里，作者发现了一个长链非编码mRNA，通过分离miR-125b促进肌肉形成，导致胰岛素样生长因子2的表达增加。
Recent studies indicate important roles for long noncoding RNAs (lncRNAs) as essential regulators of myogenesis and adult skeletal muscle regeneration. However, the specific roles of lncRNAs in myogenic differentiation of adult skeletal muscle stem cells and myogenesis are still largely unknown. Here we identify a lncRNA that is specifically enriched in skeletal muscle (myogenesis-associated lncRNA, in short, lnc-mg). In mice, conditional knockout of lnc-mg in skeletal muscle results in muscle atrophy and the loss of muscular endurance during exercise. Alternatively, skeletal muscle-specific overexpression of lnc-mg promotes muscle hypertrophy. In vitro analysis of primary skeletal muscle cells shows that lnc-mg increases gradually during myogenic differentiation and its overexpression improves cell differentiation. Mechanistically, lnc-mg promotes myogenesis, by functioning as a competing endogenous RNA (ceRNA) for microRNA-125b to control protein abundance of insulin-like growth factor 2. These findings identify lnc-mg as a novel noncoding regulator for muscle cell differentiation and skeletal muscle development. Long non-coding mRNAs play important roles in muscle development and regeneration. Here the authors identify a long non-coding mRNA that promotes myogenesis by sequestering miR-125b, leading to increased expression of insulin-like growth factor 2.