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Autophagy protects against PI3K/Akt/mTOR-mediated apoptosis of spinal cord neurons after mechanical injury

Wang, ZhenYu, Zhou, LinQuan, Zheng, XiaoTing, Chen, Gang, Pan, RongFeng, Li, JinHuang, Liu, WenGe·2017·Neuroscience Letters
DOI 10.1016/j.neulet.2017.07.036
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Abstract

Many studies have indicated that autophagy and apoptosis play an important role in the pathogenesis of spinal cord injury. In recent years, research on autophagy-related signal transduction pathways has demonstrated that the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway is closely associated with the initiation of autophagy. However, the mechanism of the pathological relationship between this signaling pathway and apoptosis in spinal cord injury is unclear. In this study, we used an in vitro model of spinal cord injury to observe the mechanism of the PI3K/Akt/mTOR signaling pathway and the apoptosis of neurons via the mitochondrial pathway. Mitochondrial pathway apoptosis-related proteins were detected by western blot. Akt and mTOR phosphorylation levels peaked 4h after mechanical damage and then decreased. Following administration of the PI3K-specific inhibitor LY294002, the phosphorylation levels of Akt and mTOR decreased, and the ratio of autophagy-specific protein microtubule-associated protein 1 light chain (LC3)II/I was higher in the inhibitor-treated injury group than in the simple-injury group. TUNEL staining was used to detect apoptosis, and apoptosis was significantly reduced after the inhibition of the PI3K/Akt/mTOR signaling pathway. In summary, the PI3K/Akt/mTOR signaling pathway is involved in the apoptosis of neurons after mechanical injury and can induce apoptosis through the mitochondrial pa…

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Research works printed but not linked: 33

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Metadata

Authors
Wang, Z., Zhou, L., Zheng, X., Chen, G., Pan, R., Li, J., & Liu, W.
Venue
Neuroscience Letters
Publisher
Elsevier BV
Published
2017-08
Volume
656
Pages
158-164
ISSN
0304-3940
DOI
10.1016/j.neulet.2017.07.036
Cited by
74
References
4
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Funders
National Natural Science Foundation of China (81371343, 81541035)

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