期刊
CELLS
卷 10, 期 8, 页码 -出版社
MDPI
DOI: 10.3390/cells10082083
关键词
fibromodulin; myostatin; muscle aging; sarcopenia; skeletal muscle
类别
资金
- Basic Science Research Program through the National Research Foundation of Korea (NRF) - Korean Ministry of Education [2020R1A6A1A03044512]
- NRF - Korean government (MSIP) [NRF-2021R1A2C2004177, NRF-2019R1C1C1006542]
The study found that FMOD inhibits muscle aging by negatively regulating MSTN gene expression or suppressing MSTN protein, while MSTN promotes muscle aging by positively regulating the expressions of Atrogin1, CD36, and PPAR gamma genes in muscle.
The objective of this study was to investigate fibromodulin (FMOD) and myostatin (MSTN) gene expressions during skeletal muscle aging and to understand their involvements in this process. The expressions of genes related to muscle aging (Atrogin 1 and Glb1), diabetes (RAGE and CD163), and lipid accumulation (CD36 and PPAR gamma) and those of FMOD and MSTN were examined in CTX-injected, aged, MSTN-/-, and high-fat diet (HFD) mice and in C2C12 myoblasts treated with ceramide or grown under adipogenic conditions. Results from CTX-injected mice and gene knockdown experiments in C2C12 cells suggested the involvement of FMOD during muscle regeneration and myoblast proliferation and differentiation. Downregulation of the FMOD gene in MSTN-/- mice, and MSTN upregulation and FMOD downregulation in FMOD and MSTN knockdown C2C12 cells, respectively, during their differentiation, suggested FMOD negatively regulates MSTN gene expression, and MSTN positively regulates FMOD gene expression. The results of our in vivo and in vitro experiments indicate FMOD inhibits muscle aging by negatively regulating MSTN gene expression or by suppressing the action of MSTN protein, and that MSTN promotes muscle aging by positively regulating the expressions of Atrogin1, CD36, and PPAR gamma genes in muscle.
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