Korean J Physiol Pharmacol 2023; 27(3): 277-287
Published online May 1, 2023 https://doi.org/10.4196/kjpp.2023.27.3.277
Copyright © Korean J Physiol Pharmacol.
Mai Thi Nguyen1 and Wan Lee1,2,*
1Department of Biochemistry, Dongguk University College of Medicine, Gyeongju 38066, 2Channelopathy Research Center (CRC), Dongguk University College of Medicine, Goyang 10326, Korea
Correspondence to:Wan Lee
Author contributions: W.L. and M.T.N. conceived and designed the experiments. M.T.N. performed the experiments and analyzed the data. W.L. wrote the manuscript. All authors read and approved the final manuscript.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Actin dynamics play an essential role in myogenesis through multiple mechanisms, such as mechanotransduction, cell proliferation, and myogenic differentiation. Twinfilin-1 (TWF1), an actin-depolymerizing protein, is known to be required for the myogenic differentiation of progenitor cells. However, the mechanisms by which they epigenetically regulate TWF1 by microRNAs under muscle wasting conditions related to obesity are almost unknown. Here, we investigated the role of miR-103-3p in TWF1 expression, actin filament modulation, proliferation, and myogenic differentiation of progenitor cells. Palmitic acid, the most abundant saturated fatty acid (SFA) in the diet, reduced TWF1 expression and impeded myogenic differentiation of C2C12 myoblasts, while elevating miR-103-3p levels in myoblasts. Interestingly, miR-103-3p inhibited TWF1 expression by directly targeting its 3’UTR. Furthermore, ectopic expression of miR-103-3p reduced the expression of myogenic factors, i.e., MyoD and MyoG, and subsequently impaired myoblast differentiation. We demonstrated that miR-103-3p induction increased filamentous actin (F-actin) and facilitated the nuclear translocation of Yes-associated protein 1 (YAP1), thereby stimulating cell cycle progression and cell proliferation. Hence, this study suggests that epigenetic suppression of TWF1 by SFA-inducible miR-103-3p impairs myogenesis by enhancing the cell proliferation triggered by F-actin/YAP1.
Keywords: Actin cytoskeleton, miR-103-3p, Myogenesis, Twinfilin-1, YAP1
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