MiR-141-3p regulates myogenic differentiation in C2C12 myoblasts via CFL2-YAP-mediated mechanotransduction
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Skeletal myogenesis is essential to keep muscle mass and integrity,and impaired myogenesis is closely related to the etiologyof muscle wasting. Recently, miR-141-3p has been shown tobe induced under various conditions associated with musclewasting, such as aging, oxidative stress, and mitochondrial dysfunction. However, the functional significance and mechanismof miR-141-3p in myogenic differentiation have not been exploredto date. In this study, we investigated the roles of miR-141-3pon CFL2 expression, proliferation, and myogenic differentiationin C2C12 myoblasts. MiR-141-3p appeared to target the 3’UTRof CFL2 directly and suppressed the expression of CFL2, anessential factor for actin filament (F-actin) dynamics. Transfectionof miR-141-3p mimic in myoblasts increased F-actin formationand augmented nuclear Yes-associated protein (YAP), a keycomponent of mechanotransduction. Furthermore, miR-141-3pmimic increased myoblast proliferation and promoted cell cycleprogression throughout the S and G2/M phases. Consequently,miR-141-3p mimic led to significant suppressions of myogenicfactors expression, such as MyoD, MyoG, and MyHC, and hinderedthe myogenic differentiation of myoblasts. Thus, this studyreveals the crucial role of miR-141-3p in myogenic differentiationvia CFL2-YAP-mediated mechanotransduction and providesimplications of miRNA-mediated myogenic regulation in skeletalmuscle homeostasis.
Abstract
Skeletal myogenesis is essential to keep muscle mass and integrity,and impaired myogenesis is closely related to the etiologyof muscle wasting. Recently, miR-141-3p has been shown tobe induced under various conditions associated with musclewasting, such as aging, oxidative stress, and mitochondrial dysfunction. However, the functional significance and mechanismof miR-141-3p in myogenic differentiation have not been exploredto date. In this study, we investigated the roles of miR-141-3pon CFL2 expression, proliferation, and myogenic differentiationin C2C12 myoblasts. MiR-141-3p appeared to target the 3’UTRof CFL2 directly and suppressed the expression of CFL2, anessential factor for actin filament (F-actin) dynamics. Transfectionof miR-141-3p mimic in myoblasts increased F-actin formationand augmented nuclear Yes-associated protein (YAP), a keycomponent of mechanotransduction. Furthermore, miR-141-3pmimic increased myoblast proliferation and promoted cell cycleprogression throughout the S and G2/M phases. Consequently,miR-141-3p mimic led to significant suppressions of myogenicfactors expression, such as MyoD, MyoG, and MyHC, and hinderedthe myogenic differentiation of myoblasts. Thus, this studyreveals the crucial role of miR-141-3p in myogenic differentiationvia CFL2-YAP-mediated mechanotransduction and providesimplications of miRNA-mediated myogenic regulation in skeletalmuscle homeostasis.
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