Qin Fuchuang, He Guorong, Sun Yu, Chen Guangning, Yu Qijian, Ma Xilie
Department of Neurosurgery, Shulan (Anji) Hospital, Anji County, Huzhou 313300, Zhejiang, China.
Department of Neurosurgery, Xixi Hospital of Hangzhou, Hangzhou 310023, Zhejiang, China.
Chin J Physiol. 2022 Nov-Dec;65(6):282-289. doi: 10.4103/0304-4920.360035.
Spinal cord injury (SCI) is a common central nervous system disease. It is reported that long non-coding RNA LINC00158 is involved in the process of SCI. The purpose of this study was to explore the biological role of LINC00158 in the SCI. First, we established a rat SCI model by surgical method and evaluated the motor function of rats by the Basso-Beattie-Bresnahan locomotor rating scale. The results showed that the expression of LINC00158 decreased and apoptotic cells increased in the SCI model rats. Meanwhile, we found the upregulated LC3-II/LC3-I, Beclin-1, and p62 in the SCI rats. Then, primary rat spinal cord neurons were exposed to oxygen/glucose deprivation (OGD) as an in vitro cell model of SCI. After OGD treatment, the expression of LINC00158 decreased significantly and the apoptosis of spinal cord neurons increased. OGD treatment resulted in upregulation of LC3-II/LC3-I and Beclin-1 and downregulation of p62 in primary spinal cord neurons, which could be eliminated by overexpression of LINC00158. 3-Methyladenine and chloroquine (autophagy inhibitor) reversed the inhibitory effect of LINC00158 overexpression on apoptosis of primary spinal cord neurons. In conclusion, this study demonstrated that LINC00158 overexpression repressed neuronal apoptosis by promoting autophagy, suggesting that LINC00158 may be a potential therapeutic target in the SCI.
脊髓损伤（SCI）是一种常见的中枢神经系统疾病。据报道，长链非编码RNA LINC00158参与脊髓损伤过程。本研究的目的是探讨LINC00158在脊髓损伤中的生物学作用。首先，我们通过手术方法建立大鼠脊髓损伤模型，并通过Basso-Beattie-Bresnahan运动评分量表评估大鼠的运动功能。结果显示，脊髓损伤模型大鼠中LINC00158的表达降低，凋亡细胞增加。同时，我们发现脊髓损伤大鼠中LC3-II/LC3-I、Beclin-1和p62上调。然后，将原代大鼠脊髓神经元暴露于氧/葡萄糖剥夺（OGD），作为脊髓损伤的体外细胞模型。OGD处理后，LINC00158的表达显著降低，脊髓神经元凋亡增加。OGD处理导致原代脊髓神经元中LC3-II/LC3-I和Beclin-1上调，p62下调，而LINC00158的过表达可消除这种变化。3-甲基腺嘌呤和氯喹（自噬抑制剂）逆转了LINC00158过表达对原代脊髓神经元凋亡的抑制作用。总之，本研究表明LINC00158过表达通过促进自噬抑制神经元凋亡，提示LINC00158可能是脊髓损伤的潜在治疗靶点。
