Cyclic mechanical stretch promotes energy metabolism in osteoblast-like cells through an mTOR signaling-associated mechanism
- Zhaobin Zeng
- Da Jing
- Xiaodong Zhang
- Yinzhong Duan
- Feng Xue
Affiliations: State Key Laboratory of Military Stomatology, Department of Orthodontics, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi 710032, P.R. China, Department of Biomedical Engineering, The Fourth Military Medical University, Xi'an, Shaanxi 710032, P.R. China, Department of Stomatology, General Hospital of Shenyang Military Area Command, Shenyang, Liaoning 110015, P.R. China
- Published online on: August 5, 2015 https://doi.org/10.3892/ijmm.2015.2304
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Energy metabolism is essential for maintaining function and substance metabolism in osteoblasts. However, the role of cyclic stretch in regulating osteoblastic energy metabolism and the underlying mechanisms remain poorly understood. In this study, we found that cyclic stretch (10% elongation at 0.1 Hz) significantly enhanced glucose consumption, lactate levels (determined using a glucose/lactate assay kit), intracellular adenosine triphosphate (ATP) levels (quantified using rLuciferase/Luciferin reagent) and the mRNA expression of energy metabolism-related enzymes [mitochondrial ATP synthase, L-lactate dehydrogenase A (LDHA) and enolase 1; measured by RT-qPCR], and increased the phosphorylation levels of Akt, mammalian target of rapamycin (mTOR) and p70s6k (measured by western blot analysis) in human osteoblast‑like MG‑63 cells. Furthermore, the inhibition of Akt or mTOR with an antagonist (wortmannin or rapamycin) suppressed the stretch-induced increase in glucose consumption, lactate levels, intracellular ATP levels and the expression of mitochondrial ATP synthase and LDHA, indicating the significance of the Akt/mTOR/p70s6k pathway in regulating osteoblastic energy metabolism in response to mechanical stretch. Thus, we concluded that cyclic stretch regulates energy metabolism in MG‑63 cells partially through the Akt/mTOR/p70s6k signaling pathway. The present findings provide novel insight into osteoblastic mechanobiology from the perspective of energy metabolism.