Overexpression of long non-coding RNA LINC00158 inhibits neuronal apoptosis by promoting autophagy in spinal cord injury.

IF 16.4 1区化学 Q1 CHEMISTRY, MULTIDISCIPLINARY

Accounts of Chemical Research Pub Date : 2022-11-01 DOI:10.4103/0304-4920.360035

Fuchuang Qin, Guorong He, Yu Sun, Guangning Chen, Qijian Yu, Xilie Ma

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引用次数: 1

Abstract

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.

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长链非编码RNA LINC00158过表达通过促进脊髓损伤自噬抑制神经元凋亡。

脊髓损伤是一种常见的中枢神经系统疾病。据报道，长链非编码RNA LINC00158参与了SCI的发生过程。本研究的目的是探讨LINC00158在SCI中的生物学作用。首先，采用手术方法建立大鼠脊髓损伤模型，采用Basso-Beattie-Bresnahan运动评定量表对大鼠的运动功能进行评价。结果表明，在脊髓损伤模型大鼠中，LINC00158表达降低，凋亡细胞增多。同时，我们发现脊髓损伤大鼠LC3-II/LC3-I、Beclin-1和p62表达上调。然后，将原代大鼠脊髓神经元暴露于氧/葡萄糖剥夺(OGD)中作为脊髓损伤的体外细胞模型。OGD处理后，LINC00158表达明显降低，脊髓神经元凋亡增加。OGD处理导致原代脊髓神经元LC3-II/LC3-I和Beclin-1表达上调，p62表达下调，可通过过表达LINC00158消除。3-甲基腺苷和氯喹(自噬抑制剂)可逆转LINC00158过表达对原代脊髓神经元凋亡的抑制作用。综上所述，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。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Accounts of Chemical Research 化学-化学综合

CiteScore

31.40

自引率

1.10%

发文量

312

审稿时长

2 months

期刊介绍： Accounts of Chemical Research presents short, concise and critical articles offering easy-to-read overviews of basic research and applications in all areas of chemistry and biochemistry. These short reviews focus on research from the author’s own laboratory and are designed to teach the reader about a research project. In addition, Accounts of Chemical Research publishes commentaries that give an informed opinion on a current research problem. Special Issues online are devoted to a single topic of unusual activity and significance. Accounts of Chemical Research replaces the traditional article abstract with an article "Conspectus." These entries synopsize the research affording the reader a closer look at the content and significance of an article. Through this provision of a more detailed description of the article contents, the Conspectus enhances the article's discoverability by search engines and the exposure for the research.