长非编码 RNA Irm 通过与 MEF2D 相互作用增强成肌分化。
Long non-coding RNA Irm enhances myogenic differentiation by interacting with MEF2D.
机构信息
State Key Laboratory for Molecular Biology of Special Economic Animals, Institute of Special Animal and Plant Sciences, Chinese Academy of Agricultural Sciences, Changchun, 130112, China.
Joint Surgery Department, No.1 Hospital of Jilin University, Changchun, 130021, China.
出版信息
Cell Death Dis. 2019 Feb 21;10(3):181. doi: 10.1038/s41419-019-1399-2.
Recent studies suggest important roles for long non-coding RNAs as essential regulators of myogenic differentiation. Here, we report that lncRNA Irm is upregulated during myogenesis. Functional analyses show that the overexpression of Irm enhances myogenic differentiation, whereas the inhibition of Irm has completely opposite effects in vitro. Notably, the inhibition of Irm blocks damage-induced muscle regeneration in vivo. Mechanistically, Irm regulates the expression of myogenic genes by directly binding to MEF2D, which in turn promotes the assembly of MyoD/MEF2D on the regulatory elements of target genes. Collectively, we have identified a novel lncRNA that interacts with MEF2D to regulate myogenesis.
最近的研究表明，长非编码 RNA 作为肌生成分化的重要调节因子具有重要作用。在这里，我们报告 lncRNA Irm 在肌生成过程中上调。功能分析表明，Irm 的过表达增强了肌生成分化，而 Irm 的抑制在体外则具有完全相反的效果。值得注意的是，Irm 的抑制阻止了体内损伤诱导的肌肉再生。从机制上讲，Irm 通过直接与 MEF2D 结合来调节肌生成基因的表达，从而促进 MyoD/MEF2D 在靶基因的调节元件上的组装。总的来说，我们已经确定了一种与 MEF2D 相互作用以调节肌生成的新型 lncRNA。
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