RESULTS: Leu addition promoted C2C12 cell differentiation compared to the control, enhancing early differentiation via myogenic determinant (MYOD) up-regulation. Sequencing revealed SESN2 binding to and interacting with RPN2. RPN2 overexpression up-regulated MYOD, myogenin and myosin heavy chain 2, concurrently decreased p-GSK3β and increased nuclear β-catenin. Conversely, RPN2 knockdown yielded opposite results. Combining RPN2 knockdown with Leu rescued increased p-GSK3β and decreased nuclear β-catenin compared to Leu absence. Hematoxylin and eosin staining results showed that Leu addition accelerated mouse muscle damage repair, up-regulating Pax7, MYOD and RPN2 in the cytoplasm, and nuclear β-catenin, confirming that the role of Leu in muscle injury repair was consistent with the results for C2C12 cells.
CONCLUSIONS: Leu, bound with SESN2, up-regulated RPN2 expression, activated the GSK3β/β-catenin pathway, enhanced C2C12 differentiation and expedited skeletal muscle damage repair. © 2024 Society of Chemical Industry.
结果:与对照组相比,添加Leu可促进C2C12细胞分化,通过MYOD上调促进早期分化。测序显示SESN2与RPN2结合并相互作用。RPN2过表达上调MYOD,MYOG,和MYH2,同时降低p-GSK3β,核β-连环蛋白增加。相反,RPN2敲低产生相反的结果。与不存在Leu相比,将RPN2敲低与Leu相结合可挽救增加的p-GSK3β和减少的核β-连环蛋白。HE染色结果显示添加Leu加速小鼠肌肉损伤修复,上调Pax7,MYOD,细胞质中的RPN2,和核β-连环蛋白,证实Leu在肌肉损伤修复中的作用与C2C12细胞的结果一致。
结论:列伊,与SESN2结合,上调RPN2表达,激活GSK3β/β-catenin通路,增强C2C12分化,加速骨骼肌损伤修复。本文受版权保护。保留所有权利。