beta-Hydroxy-beta-methylbutyrate-Induced Upregulation of miR-199a-3p Contributes to Slow-To-Fast Muscle Fiber Type Conversion in Mice and C2C12 Cells

文献类型： 外文期刊

第一作者： Zhang, Yong

作者： Zhang, Yong;Zhou, Pan;Yan, Honglin;Zhang, Zhenzhen;Zhang, Hongfu;Liu, Jingbo;Yang, Min;Zhang, Hongfu;Liu, Jingbo;Qi, Renli

作者机构：

关键词： HMB; myofiber type transition; mice; C2C12 cells; miR-199a-3p; TEAD1

期刊名称：JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY （ 影响因子：5.279； 五年影响因子：5.269 ）

ISSN： 0021-8561

年卷期： 2020 年 68 卷 2 期

页码：

收录情况： SCI

摘要： The influence of beta-hydroxy-beta-methylbutyrate (HMB) on proliferation and differentiation of myogenic cells has been well-studied. However, the role of HMB in myofiber specification and potential mechanisms is largely unknown. Thus, the objective of this research was to explore the role of HMB supplementation in myofiber specification. Results showed that HMB treatment significantly increased the fast MyHC protein level (mice: 1.59 +/- 0.08, P < 0.01; C2C12: 2.26 +/- 0.11, P < 0.001), decreased the slow MyHC protein level (mice: 0.76 +/- 0.05, P < 0.05; C2C12: 0.52 +/- 0.02, P < 0.001), and increased the miR-199a-3p level (mice: 4.93 +/- 0.37, P < 0.001; C2C12: 11.25 +/- 0.57, P < 0.001). Besides, we also observed that HMB promoted the activity of glycolysis-related enzymes and reduced the activities of oxidation-related enzymes in mice and C2C12 cells. Overexpression of miR-199a-3p downregulated the slow MyHC protein level (0.71 +/- 0.02, P < 0.01) and upregulated the fast MyHC protein level (2.13 +/- 0.09, P < 0.001), while repression of miR-199a-3p exhibited the opposite effect. Target identification results verified that miR-199a-3p targets the 3'UTR of the TEA domain family member 1 (TEAD1) to cause its post-transcriptional inhibition (0.41 +/- 0.07, P < 0.01). Knockdown of TEAD1 exhibited a similar effect with miR-199a-3p on myofiber specification. Moreover, suppression of miR-199a-3p blocked slow-to-fast myofiber type transition induced by HMB. Together, our finding revealed that miR-199-3p is induced by HMB and contributes to the action of HMB on slow-to-fast myofiber type conversion via targeting TEAD1.

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