Phosphorylated GSK‑3β protects stress‑induced apoptosis of myoblasts via the PI3K/Akt signaling pathway.

Facial jaw muscle is involved in the occurrence, development, treatment and maintenance of maxillofacial deformities. The structure and function of this tissue can be altered by changes in external stimuli, and orthodontists can regulate its reconstruction using orthopedic forces. The PI3K/Akt signaling pathway is most well‑known for its biological functions in cell proliferation, survival and apoptosis. In the present study, the effects of the PI3K/Akt signaling pathway in cyclic stretch‑induced myoblast apoptosis were investigated. For this purpose, L6 rat myoblasts were cultured under mechanical stimulation and treated with the PI3K kinase inhibitor, LY294002, to elucidate the role of the PI3K/Akt signaling pathway. Cells were stained with Hoechst 33258 to visualize morphological changes and apoptosis of myoblasts, and western blotting was performed to detect expression of Akt, phosphorylated (p)‑Akt (Ser473), glycogen synthase kinase 3β (GSK‑3β) and p‑GSK‑3β (Ser9). After addition of PI3K inhibitor, the expression of total Akt and GSK‑3β did not significantly differ among groups; however, the levels of p‑Akt and p‑GSK‑3β were lower in inhibitor‑treated groups than in those treated with loading stress alone. In addition, the rate of apoptosis in myoblasts subjected to cyclic stretch increased in a time‑dependent manner, peaking at 24 h. Collectively, it was also demonstrated that the PI3K/Akt/GSK‑3β pathway plays an important role in stretch‑induced myoblast apoptosis.

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