Pb inhibited C2C12 myoblast differentiation by regulating HDAC2

被引:1
作者
Gu, Xiaozhen [1 ,2 ]
Shen, Nan [1 ,2 ]
Huang, Chengqing [1 ,2 ]
Wang, Hui-Li [1 ,2 ]
机构
[1] Hefei Univ Technol, Engn Res Ctr Bioproc, Minist Educ, 193 Tunxi Rd, Hefei 230009, Anhui, Peoples R China
[2] Hefei Univ Technol, Sch Food & Biol Engn, 193 Tunxi Rd, Hefei 230009, Peoples R China
基金
美国国家科学基金会;
关键词
Pb; Proliferation; Myoblasts differentiation; HDAC2; MUSCLE;
D O I
10.1016/j.tox.2023.153639
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Myogenesis is a crucial process governing skeletal muscle development and homeostasis. Lead (Pb) exposure impaired the development and the health of bones, which slows the growth of children. However, it is far from clear what exactly the effects of Pb on skeletal muscle development are. In this study, C2C12 cells are commonly used as an in vitro model of muscle regeneration due to their ability to transition from a proliferative phase into differentiated myofibers. The dose of 1, 5, and 10 mu M Pb were adopted to study the toxicity of Pb on C2C12 proliferation and differentiation. First, the effects of Pb on cell viability were detected and the results demonstrated that 5 mu M and 10 mu M Pb exposure decreased cell viability, while 1 mu M Pb exposure has no obvious effects on cell viability. Then, 1-10 mu M Pb exposure seriously reduced the C2C12 myoblasts differentiation, with the decrease of myogenic differentiation marker genes expression, including Muscle creatine kinase (MCK), Myosin Heavy Chain 4 (MYH4), Myogenin (MYOG), Myogenic Differentiation (MYOD). What's more, it was found that the epigenetic modifier histone deacetylase-2 (HDAC2) was upregulated after Pb exposure on C2C12 myoblasts. Further studies conclusively showed knockdown of HDAC2 ameliorated Pb-damaged C2C12 myoblasts differentiation, indicating HDAC2 plays a vital role in the Pb-induced C2C12 myoblasts differentiation deficits. In summary, these results demonstrated that Pb exposure inhibited C2C12 myoblasts differentiation by regulating HDAC2.
引用
收藏
页数:9
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