Abstract
Numerous studies have established the critical roles of microRNAs in regulating post-transcriptional gene expression in diverse biological processes. Here, we report on the role and mechanism of miR-24-3p in skeletal muscle differentiation and regeneration. miR-24-3p promotes myoblast differentiation and skeletal muscle regeneration by directly targeting high mobility group AT-hook 1 (HMGA1) and regulating it and its direct downstream target, the inhibitor of differentiation 3 (ID3). miR-24-3p knockdown in neonatal mice increases PAX7-positive proliferating muscle stem cells (MuSCs) by derepressing Hmga1 and Id3. Similarly, inhibition of miR-24-3p in the tibialis anterior muscle prevents Hmga1 and Id3 downregulation and impairs regeneration. These findings provide evidence that the miR-24-3p/HMGA1/ID3 axis is required for MuSC differentiation and skeletal muscle regeneration in vivo.
Highlights
During postnatal skeletal muscle development and regeneration, quiescent muscle stem cells (MuSCs) are activated to re-enter the cell cycle, followed by proliferation to form a pool of myoblasts, which differentiate and fuse into newly formed or existing myofibers [1]
Inhibiting miR24-3p in the tibialis anterior muscle prevents Hmga1 and Id3 downregulation and impairs regeneration. These findings provide evidence that the miR-24-3p/HMGA1/inhibitor of differentiation 3 (ID3) axis is required for MuSC differentiation and regeneration in vivo
Results miR-24-3p is abundantly expressed in adult skeletal muscle and is regulated during myoblast differentiation and skeletal muscle regeneration Using a transcription-wide screening for microRNAs, we identified several microRNAs that are differentially expressed during C2C12 myoblast differentiation [14]
Summary
During postnatal skeletal muscle development and regeneration, quiescent MuSCs are activated to re-enter the cell cycle, followed by proliferation to form a pool of myoblasts, which differentiate and fuse into newly formed or existing myofibers [1]. This extensive process of making new muscle is known as myogenesis and is essential for maintaining normal physiological function. Most of the understanding of the critical myogenic processes, including myoblast differentiation and skeletal muscle regeneration, is based on the regulation of myogenic transcription factors and signaling molecules [1-8] It is not well understood how these factors of the myogenic network are regulated to maintain normal myogenesis and skeletal muscle function. An emerging research area is exploring microRNAs’ role in post-transcriptional gene regulation during skeletal myogenesis
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