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    • Recently microRNAs miRNAs a class of conserved

    2020-07-31

    Recently, microRNAs (miRNAs), a class of conserved small non-coding RNAs [9], have emerged as novel and essential regulators of myogenesis [10]. They vary from 17 to 24 nucleotides in length and induce mRNA degradation or translation inhibition by interacting with the 3′UTRs of their target mRNAs [9]. miRNAs may regulate myogenesis by regulating the process of myoblast proliferation and differentiation [11]. miR-206 and miR-486 can cause myoblasts to exit the proliferation and MDL 12330A hydrochloride stage, and subsequently enter the differentiation phase by directly suppressing Pax7 expression [12]. Eric Olson et al. reported that several miRNAs are involved in muscle fiber type programs [13]. Especially, miR-208b and miR-499 are involved in slow-twitch fiber programming by modulating contractile protein gene expression [13,14]. Interestingly, our previous studies from porcine skeletal muscle high-throughput sequencing found that the expression of miR-204-5p gradually decreased with age [15]. Sheng et al. [16] reported that the expression of miR-204-5p was significantly increased in skeletal muscle at all postnatal stages in Min pigs, which has low lean meat percentage, compared to its expression in Large White pigs, which contains high lean meat percentage. These studies imply that miR-204-5p has a potential function in regulating muscle development. However, the role of miR-204-5p in myoblast differentiation, which is the critical process of determining muscle cell fate and final muscle formation, has not been reported yet. In the current study, we found that miR-204-5p is negatively correlated with myoblast differentiation. We suppose that miR-204-5p blunts myoblast differentiation and reduces the composition of MyHC in slow-twitch fibers by targeting MEF2C and ERRγ. We provide evidence that miR-204-5p affects myoblast differentiation.
    Materials and methods
    Results and discussion
    Conclusions In the present study, we have shown the important role of miR-204-5p in C2C12 myoblast differentiation. Overexpression of miR-204-5p inhibited myogenic differentiation and decreased the formation of slow-twitch myofibers, whereas miR-204-5p inhibitors had the opposite effect. Our results confirmed that miR-204-5p directly targets the 3′UTR of MEF2C and ERRγ. We found that interference with either MEF2C or ERRγ reduces myoblast differentiation and causes a reduction in slow-twitch myofibers. Meanwhile, either si-MEF2C or si-ERRγ co-transfected with miR-204-5p mimics caused a greater degree of attenuation of myoblast differentiation. Therefore, we have presented evidence that miR-204-5p regulates myoblast differentiation and muscle fiber types by targeting MEF2C and ERRγ. Our findings suggest that miR-204-5p might serve as a potential regulatory factor that influences myogenesis.
    Declare of conflict interest
    Conflict of interest
    Acknowledgments
    ERR Subfamily Nuclear receptors (NRs) are members of a large family of transcription factors that coordinate and regulate gene expression during various cellular processes. Most NRs are ligand dependent. However, there are a few NRs for which appropriate endogenous ligands have not yet been identified; thus, they are defined as orphan NRs. ERRs are orphan receptors consisting of three members, namely, ERRα (NR3B1), ERRβ (NR3B2), and ERRγ (NR3B3) [1]. ERRα and β, which were identified before ERRγ, have been extensively studied 1, 2, 3. ERRγ was first identified through its connection with a critical region of Usher syndrome type IIa [4], and later characterized as a protein interacting with the nuclear receptor coactivator glucocorticoid receptor-interacting protein (GRIP)-1 [5]. It is highly expressed in different fetal and adult human tissues, including the placenta, brain, skeletal muscle, heart, and liver [1]. ERRγ shares the structural features found in other members of the NR superfamily (Figure 1). It contains a N-terminal activation function (AF)-1 domain that is involved in the transcriptional regulation of the receptor and a central zinc finger DNA-binding domain (DBD) that is highly conserved among the three members. Similar to ERRα and β, the DBD of ERRγ binds to the same DNA element, TCAAGGTCA, which is defined as the ERR response element (ERRE). ERRγ also contains a ligand-binding domain (LBD), as well as a C-terminal AF-2 domain that interacts with coactivators and co-repressors [3]. As ERRγ shares nearly identical DBDs with ERRα and β, its transcriptional regulatory functions are likely similar to and overlap with those of ERRα and β in cells where they are coexpressed. For example, both ERRα and ERRγ promote oxidative capacity in skeletal and cardiac muscles 6, 7, 8. The functions of ERRβ and ERRγ are also overlapping; both NRs regulate genes important for ion homeostasis in the heart, kidney, stomach, skeletal muscle, and trophoblasts 9, 10, 11. However, ERRγ also controls metabolic processes, which do not involve ERRα and β 12, 13, 14, 15.