机构：[1]Department of Stomatology, Nanjing Tongren Hospital, School of Medicine, Southeast University, Nanjing, Jiangsu 211102[2]Department of Implantology, Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, Jiangsu 210008[3]Department of Orthodontics, The Affiliated Qingdao Municipal Hospital, Qingdao University, Qingdao, Shandong 266000, P.R. China
The PI3K/AKT signaling pathway regulates cell proliferation and differentiation in multiple types of cells. The present study aimed to investigate the effects of mechanical stress on C2C12 cell proliferation and to explore the associated mechanisms. A cyclic mechanical stress model of C2C12 myoblasts was established. Reverse transcription-quantitative PCR and western blotting assay were used to examine the PI3K signaling pathways involved in the progress of cell differentiation. Cell counting kit-8 (CCK-8) assay was used to evaluate the proliferation of C2C12 cells. Flow cytometry was employed to evaluate apoptosis following mechanical stress. The results demonstrated that mechanical stress activated the PI3K signaling pathway in C2C12 myoblasts. Mechanical stress significantly promoted phosphorylation (p-) of AKT and expression of mammalian target of rapamycin (mTOR) compared with the normal group. Mechanical stress significantly promoted 4E-binding protein 1 (4EBP1) expression in C2C12 cells compared with the normal group. The PI3K specific inhibitor LY294002 significantly decreased 4EBP1 expression and reduced p-AKT and p-mTOR expression compared with the mechanical stress group. Mechanical stress promoted C2C12 cell proliferation. Apoptosis of C2C12 significantly decreased in the mechanical stress group compared with the normal group. Cyclin D levels significantly increased in the mechanical stress group compared with the normal group. In conclusion, mechanical stress promoted biological functions of C2C12 cells by activating the PI3K/AKT signaling pathway. These results may contribute to a better understanding of the effects of mechanical stress on cells.
基金：
The Nanjing Science and
Technology Development Project (2016; grant no. 201605067).
Figure 7. Evaluation for cyclin D expression using western blot assay.
(A) Western blot analysis images. Lanes: 1‑1, normal group 24 h; 1‑2, normal
group 48 h; 1‑3, normal group 72 h; 2‑1, normal + stress group 24 h; 2‑2,
normal + stress group 48 h; and 1‑3 normal + stress group 72 h. (B) Statistical
analysis for cyclin D expression. *P<0.05 vs. normal group at different
time-points.
第一作者机构：[1]Department of Stomatology, Nanjing Tongren Hospital, School of Medicine, Southeast University, Nanjing, Jiangsu 211102
通讯作者：
通讯机构：[2]Department of Implantology, Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, Jiangsu 210008[*1]Department of Implantology, Nanjing Stomatological Hospital, Medical School of Nanjing University, 30 Zhongyang Road, Xuanwu, Nanjing, Jiangsu 210008, P.R. China
推荐引用方式(GB/T 7714)：
Da Yu,Mou Yongbin,Wang Mengjia,et al.Mechanical stress promotes biological functions of C2C12 myoblasts by activating PI3K/AKT/mTOR signaling pathway[J].MOLECULAR MEDICINE REPORTS.2020,21(1):470-477.doi:10.3892/mmr.2019.10808.
APA：
Da, Yu,Mou, Yongbin,Wang, Mengjia,Yuan, Xiao,Yan, Fuhua...&Zhang, Fang.(2020).Mechanical stress promotes biological functions of C2C12 myoblasts by activating PI3K/AKT/mTOR signaling pathway.MOLECULAR MEDICINE REPORTS,21,(1)
MLA：
Da, Yu,et al."Mechanical stress promotes biological functions of C2C12 myoblasts by activating PI3K/AKT/mTOR signaling pathway".MOLECULAR MEDICINE REPORTS 21..1(2020):470-477
