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MicroRNA?23a?5p mediates the proliferation and differentiation of C2C12 myoblasts.

ABSTRACT: Skeletal myogenesis is a highly ordered and complex biological process that is mediated by numerous regulatory factors. In previous studies, it has been demonstrated that microRNAs (miRs) and long non?coding RNAs (lncRNAs) serve key roles in skeletal myogenesis. The present study showed that the expression levels of miR?23a?5p showed a dynamic change from decrease to increase during C2C12 myoblast proliferation and differentiation. Functional analysis using 5?ethynyl?2'?deoxyuridine proliferation and Cell Counting Kit?8 detection assays indicated that overexpression of miR?23a?5p significantly promoted C2C12 myoblast proliferation compared with the negative control. In addition, in C2C12 myoblasts transfected with miR?23a?5p mimics, increased expression levels of regulators associated with cell proliferation (Cyclin E, CCND1 and Cyclin B) were observed compared with the negative control. By contrast, overexpression of miR?23a?5p decreased the expression levels of specific?myogenesis factors (MyoD, MyoG and Myf5) and decreased C2C12 myoblast differentiation. Luciferase activity assays indicated that miR?23a?5p suppressed the luciferase activity of lncDum. Further analysis demonstrated that miR?23a?5p not only showed an opposite expression level pattern compared with lncDum, which was first increased and then decreased, but also had an opposite effect on the proliferation and differentiation of C2C12 myoblasts compared with lncDum which inhibited cell proliferation and promoted cell differentiation. Taken together, these results indicated that miR?23a?5p may mediate the proliferation and differentiation of C2C12 myoblasts, which may be involved in lncDum regulation.

SUBMITTER: Zhao X

PROVIDER: S-EPMC7533443 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature

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MicroRNA‑23a‑5p mediates the proliferation and differentiation of C2C12 myoblasts.

Zhao Xue X Gu Hao H Wang Linghui L Zhang Peiwen P Du Jingjing J Shen Linyuan L Jiang Dongmei D Wang Jinyong J Li Xuewei X Zhang Shunhua S Li Mingzhou M Zhu Li L

Molecular medicine reports 20200902 5

Skeletal myogenesis is a highly ordered and complex biological process that is mediated by numerous regulatory factors. In previous studies, it has been demonstrated that microRNAs (miRs) and long non‑coding RNAs (lncRNAs) serve key roles in skeletal myogenesis. The present study showed that the expression levels of miR‑23a‑5p showed a dynamic change from decrease to increase during C2C12 myoblast proliferation and differentiation. Functional analysis using 5‑ethynyl‑2'‑deoxyuridine proliferatio ...[more]

PMID: 32901860

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Project description:In cancer patients, chemotherapeutic medication induces aberrant ROS (reactive oxygen species) accumulation in skeletal muscles, resulting in myofiber degradation, muscle weakness, and even cachexia, which further leads to poor therapeutic outcomes. Acting as an antioxidant, taurine is extensively used to accelerate postexercise muscle recovery in athletes. The antioxidant effects of taurine have been shown in mature myotubes and myofibers but not yet in myoblasts, the myotube precursor. The proliferation and differentiation ability of myoblasts play a very important role in myofiber repair and regeneration, which is usually impaired during chemotherapeutics in cancer patients as well. Here, we explored the effects of taurine supplementation on C2C12 myoblasts exposed to cisplatin-induced ROS. We found that cisplatin treatment led to dramatically decreased cell viability; accumulated ROS level; down-regulated expressions of MyoD1 (myoblast determination protein 1), myogenin, and MHC (myosin heavy chain); and impaired myotube differentiation in myoblasts. Significantly, taurine supplementation protected myoblasts against cisplatin-induced cell viability decrease, promoted cellular ROS clearance, and, most importantly, preserved the expressions of MyoD1, myogenin, and MHC as well as myotube differentiation ability. We further conducted NMR-based metabolomic analysis to clarify the underlying molecular mechanisms. We identified 14 characteristic metabolites primarily responsible for the discrimination of metabolic profiles between cisplatin-treated cells and normal counterparts, including increased levels of BCAAs (branched-chain amino acids: leucine and isoleucine), alanine, glycine, threonine, glucose, ADP (adenosine diphosphate), phenylalanine, and PC (O-phosphocholine), and decreased levels of lysine, β-alanine, choline, GPC (sn-glycero-3-phosphocholine), and myo-inositol. Evidently, taurine supplementation partially reversed the changing trends of several metabolites (isoleucine, threonine, glycine, PC, β-alanine, lysine, and myo-inositol). Furthermore, taurine supplementation promoted the proliferation and myotube differentiation of myoblasts by alleviating cellular catabolism, facilitating GSH (reduced glutathione) biosynthesis, improving glucose utilization and TCA (tricarboxylic acid) cycle anaplerosis, and stabilizing cellular membranes. Our results demonstrated the protective effects of taurine on cisplatin-impaired myoblasts and elucidated the mechanistic rationale for the use of taurine to ameliorate muscle toxicity in clinical chemotherapy cancer patients.

Dataset Information

MicroRNA?23a?5p mediates the proliferation and differentiation of C2C12 myoblasts.

Publications

MicroRNA‑23a‑5p mediates the proliferation and differentiation of C2C12 myoblasts.

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