跨膜蛋白16A（TMEM16A）激活抑制背根神经节细胞自噬，这与p38丝裂原活化蛋白激酶/雷帕霉素靶蛋白（p38 MAPK/mTOR）信号通路相关。
TMEM16A Activation Inhibits Autophagy in Dorsal Root Ganglion Cells, Which is Associated with the p38 MAPK/mTOR Pathway.
作者信息
Yang Shuyun, Shang Hui, Zhang Yuruo, Qiu Jingsong, Guo Zheyi, Ma Yong, Lan Yuhang, Cui Shaoyang, Tong Hongshuang, Li Guocai
机构信息
Department of Anesthesiology, Shenzhen Hospital (Futian) of Guangzhou University of Chinese Medicine, Shenzhen, 518034, Guangdong Province, China.
Sixth Clinical School of Medicine, Guangzhou University of Chinese Medicine, Shenzhen, 518034, Guangdong Province, China.
出版信息
Cell Mol Neurobiol. 2024 Dec 4;45(1):1. doi: 10.1007/s10571-024-01507-z.
Transmembrane member 16A (TMEM16A) exhibits a negative correlation with autophagy, though the underlying mechanism remains elusive. This study investigates the mechanism between TMEM16A and autophagy by inducing autophagy in DRG neuronal cells using Rapamycin. Results indicated that TMEM16A interference augmented cell viability and reduced Rapamycin-induced apoptosis. Autophagosome formation increased with TMEM16A interference but decreased upon overexpression. A similar increase in autophagosomes was observed with SB203580 treatment. Furthermore, TMEM16A interference suppressed Rapamycin-induced gene and protein expression of p38 MAPK and mTOR, whereas overexpression had the opposite effect. These findings suggest that TMEM16A activation inhibits autophagy in DRG cells, which is associated with the p38 MAPK/mTOR pathway, offering a potential target for mitigating neuropathic pain (NP).
跨膜蛋白16A（TMEM16A）与自噬呈负相关，但其潜在机制仍不清楚。本研究通过使用雷帕霉素诱导背根神经节（DRG）神经元细胞自噬，探讨TMEM16A与自噬之间的机制。结果表明，TMEM16A干扰增强了细胞活力，并减少了雷帕霉素诱导的细胞凋亡。TMEM16A干扰后自噬体形成增加，而过表达则减少。用SB203580处理也观察到自噬体有类似增加。此外，TMEM16A干扰抑制了雷帕霉素诱导的p38丝裂原活化蛋白激酶（p38 MAPK）和雷帕霉素靶蛋白（mTOR）的基因和蛋白表达，而过表达则有相反的效果。这些发现表明，TMEM16A激活抑制DRG细胞中的自噬，这与p38 MAPK/mTOR途径有关，为减轻神经性疼痛（NP）提供了一个潜在靶点。
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