Embryonic and neonatal skeletal muscles grow via the proliferation and fusion of myogenic cells, whereas adult skeletal muscle adapts largely by remodelling pre-existing myofibers and optimizing metabolic balance. It has been reported that miRNAs played key roles during skeletal muscle development through targeting different genes at post-transcriptional level. In this study, we show that a single miRNA (miR-208b) can modulate both the myogenesis and homoeostasis of skeletal muscle by distinct targets. As results, miR-208b accelerates the proliferation and inhibits the differentiation of myogenic cells by targeting the E-protein family member transcription factor 12 (TCF12). Also, miR-208b can stimulate fast-to-slow fibre conversion and oxidative metabolism programme through targeting folliculin interacting protein 1 (FNIP1) but not TCF12 gene. Further, miR-208b could active the AMPK/PGC-1a signalling and mitochondrial biogenesis through targeting FNIP1. Thus, miR-208b could mediate skeletal muscle development and homoeostasis through specifically targeting of TCF12 and FNIP1.

胚胎和新生儿骨骼肌通过成肌细胞的增殖和融合而生长，而成年骨骼肌则通过重塑既存的肌纤维和优化代谢平衡来适应。据报道，miRNA通过在转录后水平靶向不同基因而在骨骼肌发育中发挥关键作用。在这项研究中，我们显示了一个单一的miRNA（miR-208b）可以通过不同的靶标调节骨骼肌的成肌和稳态。结果，miR-208b通过靶向E蛋白家族成员转录因子12（TCF12）来加速增殖并抑制成肌细胞的分化。而且，miR-208b可以通过靶向卵泡蛋白相互作用蛋白1（FNIP1）而非TCF12基因来刺激快速至缓慢的纤维转化和氧化代谢程序。此外，miR-208b可以通过靶向FNIP1激活AMPK / PGC-1a信号传导和线粒体生物发生。因此，miR-208b可以通过特异性靶向TCF12和FNIP1介导骨骼肌的发育和稳态。