当前位置: X-MOL 学术Stem Cells Dev. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Oleate Ameliorates Palmitate-Induced Impairment of Differentiative Capacity in C2C12 Myoblast Cells
Stem Cells and Development ( IF 2.5 ) Pub Date : 2021-03-03 , DOI: 10.1089/scd.2020.0168
Mengjuan Xue 1, 2 , Fan Zhang 1, 2 , Xueying Ji 1, 2 , Huiyuan Yu 1, 2 , Xin Jiang 1, 2 , Yixuan Qiu 1, 2 , Jiaming Yu 1, 2 , Jie Chen 1, 2 , Fan Yang 1, 2 , Zhijun Bao 1, 2
Affiliation  

A common observation in metabolic disorders and aging is the elevation of free fatty acids (FFAs), which can form ectopic fat deposition and result in lipotoxicity. Ectopic fat deposition of skeletal muscle has been recognized as an important component of aging, frailty, and sarcopenia. Previous studies have suggested that lipotoxicity caused by FFAs mainly stemmed from saturated fatty acids and decreased unsaturated/saturated fatty acid ratio in serum are also observed among metabolic disorder patients. However, the different effects of saturated fatty acids and unsaturated fatty acids on skeletal muscle are not fully elucidated. In this study, we verified that palmitate (PA), a saturated fatty acid, could lead to impaired differentiative capacity of C2C12 myoblasts by affecting Pax7, MyoD, and myogenin (MyoG), which are master regulators of lineage specification and the myogenic program. Then, oleate (OA), a monounsaturated fatty acid, were added to culture medium together with PA. Results showed that OA could ameliorate the impairment of differentiative capacity in C2C12 myoblast cells. In addition, we found PI3K/Akt signaling pathway played an important role during the process by RNA sequencing and bioinformatics analysis. The positive effect of OA on myoblast differentiative capacity disappeared if PI3K inhibitor LY294002 was added. In conclusion, our study showed that PA could destroy differentiative capacity of C2C12 myoblasts by affecting the expression of Pax7, MyoD, and MyoG, and OA could improve this impairment through PI3K/Akt signaling pathway.

中文翻译:

油酸改善棕榈酸诱导的 C2C12 成肌细胞分化能力受损

代谢紊乱和衰老的一个常见观察结果是游离脂肪酸 (FFA) 的升高,可形成异位脂肪沉积并导致脂毒性。骨骼肌的异位脂肪沉积已被认为是衰老、虚弱和肌肉减少症的重要组成部分。先前的研究表明,在代谢紊乱患者中也观察到由​​ FFAs 引起的脂毒性主要源于饱和脂肪酸和血清中不饱和/饱和脂肪酸比率降低。然而,饱和脂肪酸和不饱和脂肪酸对骨骼肌的不同作用尚未完全阐明。在这项研究中,我们证实棕榈酸酯 (PA) 是一种饱和脂肪酸,可通过影响 Pax7、MyoD 和肌细胞生成素 (MyoG) 导致 C2C12 成肌细胞的分化能力受损,它们是谱系规范和生肌程序的主要调节器。然后,油酸 (OA),一种单不饱和脂肪酸,与 PA 一起添加到培养基中。结果表明OA可以改善C2C12成肌细胞分化能力的损害。此外,我们通过RNA测序和生物信息学分析发现PI3K/Akt信号通路在这一过程中发挥了重要作用。如果加入 PI3K 抑制剂 LY294002,OA 对成肌细胞分化能力的积极影响就会消失。总之,我们的研究表明,PA 可以通过影响 Pax7、MyoD 和 MyoG 的表达来破坏 C2C12 成肌细胞的分化能力,而 OA 可以通过 PI3K/Akt 信号通路改善这种损伤。与 PA 一起加入培养基中。结果表明OA可以改善C2C12成肌细胞分化能力的损害。此外,我们通过RNA测序和生物信息学分析发现PI3K/Akt信号通路在这一过程中发挥了重要作用。如果加入 PI3K 抑制剂 LY294002,OA 对成肌细胞分化能力的积极影响就会消失。总之,我们的研究表明,PA 可以通过影响 Pax7、MyoD 和 MyoG 的表达来破坏 C2C12 成肌细胞的分化能力,而 OA 可以通过 PI3K/Akt 信号通路改善这种损伤。与 PA 一起加入培养基中。结果表明OA可以改善C2C12成肌细胞分化能力的损害。此外,我们通过RNA测序和生物信息学分析发现PI3K/Akt信号通路在这一过程中发挥了重要作用。如果加入 PI3K 抑制剂 LY294002,OA 对成肌细胞分化能力的积极影响就会消失。总之,我们的研究表明,PA 可以通过影响 Pax7、MyoD 和 MyoG 的表达来破坏 C2C12 成肌细胞的分化能力,而 OA 可以通过 PI3K/Akt 信号通路改善这种损伤。我们通过RNA测序和生物信息学分析发现PI3K/Akt信号通路在这一过程中发挥了重要作用。如果加入 PI3K 抑制剂 LY294002,OA 对成肌细胞分化能力的积极影响就会消失。总之,我们的研究表明,PA 可以通过影响 Pax7、MyoD 和 MyoG 的表达来破坏 C2C12 成肌细胞的分化能力,而 OA 可以通过 PI3K/Akt 信号通路改善这种损伤。我们通过RNA测序和生物信息学分析发现PI3K/Akt信号通路在这一过程中发挥了重要作用。如果加入 PI3K 抑制剂 LY294002,OA 对成肌细胞分化能力的积极影响就会消失。总之,我们的研究表明,PA 可以通过影响 Pax7、MyoD 和 MyoG 的表达来破坏 C2C12 成肌细胞的分化能力,而 OA 可以通过 PI3K/Akt 信号通路改善这种损伤。
更新日期:2021-03-05
down
wechat
bug