Autophagy protects nucleus pulposus cells from cyclic mechanical tension‑induced apoptosis.

Intervertebral disc (IVD) degeneration (IDD) is considered to be a primary cause of lower back pain. Mechanical stress is one of the most important factors affecting IDD. It has been demonstrated that apoptosis is important in the decrease of functional IVD cells, and that mechanical stress influences disc cell apoptosis. Autophagy, an adaptive response of the cells to survival when faced with different conditions of stress, has been documented in IDD. Apoptosis and autophagy share the same stimuli and regulatory proteins, but have different threshold responses. Recently, cyclic mechanical tension (CMT) has been shown to influence IVD cell apoptosis and autophagy. However, the conversion and coordination between apoptosis and autophagy induced by CMT remains to be fully elucidated. In the present study, it was found that CMT with 20% elongation generated by the Flexercell Tension system induced the apoptosis of nucleus pulposus (NP) cells in a time‑dependent manner. When the cells were stretched for >6 h, autophagy was increased, and showed a tendency to decrease with the duration of CMT. The autophagic activity of NP cells was partially decreased by 3‑MA and was not significantly regulated by rapamycin. CMT‑induced apoptosis was partially enhanced by the decreased autophagic activity induced by 3‑MA. In addition, the level of reactive oxygen species (ROS) in NP cells induced by CMT was significantly upregulated by 3‑MA. These results suggested that abnormal mechanical stress enhanced disc cell apoptosis and consequently accelerated the process of IDD. Autophagy helps to protect against CMT‑induced apoptosis in disc cells and ROS may be important in this process. These findings are beneficial for further understanding the mechanism of disc cell apoptosis and autophagy.