Mechanical stress promotes biological functions of C2C12 myoblasts by activating PI3K/AKT/mTOR signaling pathway

  • Authors:
    • Yu Da
    • Yongbin Mou
    • Mengjia Wang
    • Xiao Yuan
    • Fuhua Yan
    • Weidong Lan
    • Fang Zhang
  • View Affiliations

  • Published online on: November 11, 2019     https://doi.org/10.3892/mmr.2019.10808
  • Pages: 470-477
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

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.
View Figures
View References

Related Articles

Journal Cover

January-2020
Volume 21 Issue 1

Print ISSN: 1791-2997
Online ISSN:1791-3004

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Da Y, Mou Y, Wang M, Yuan X, Yan F, Lan W and Zhang F: Mechanical stress promotes biological functions of C2C12 myoblasts by activating PI3K/AKT/mTOR signaling pathway. Mol Med Rep 21: 470-477, 2020
APA
Da, Y., Mou, Y., Wang, M., Yuan, X., Yan, F., Lan, W., & Zhang, F. (2020). Mechanical stress promotes biological functions of C2C12 myoblasts by activating PI3K/AKT/mTOR signaling pathway. Molecular Medicine Reports, 21, 470-477. https://doi.org/10.3892/mmr.2019.10808
MLA
Da, Y., Mou, Y., Wang, M., Yuan, X., Yan, F., Lan, W., Zhang, F."Mechanical stress promotes biological functions of C2C12 myoblasts by activating PI3K/AKT/mTOR signaling pathway". Molecular Medicine Reports 21.1 (2020): 470-477.
Chicago
Da, Y., Mou, Y., Wang, M., Yuan, X., Yan, F., Lan, W., Zhang, F."Mechanical stress promotes biological functions of C2C12 myoblasts by activating PI3K/AKT/mTOR signaling pathway". Molecular Medicine Reports 21, no. 1 (2020): 470-477. https://doi.org/10.3892/mmr.2019.10808