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Year : 2022  |  Volume : 65  |  Issue : 6  |  Page : 282-289

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

1 Department of Neurosurgery, Shulan (Anji) Hospital, Anji County, Huzhou 313300, Zhejiang, China
2 Department of Neurosurgery, Xixi Hospital of Hangzhou, Hangzhou 310023, Zhejiang, China
3 Department of Neurosurgery, Zhejiang Chinese Medical University, Hangzhou 310053, Zhejiang, China
4 Department of Osteology, Hangzhou Red Cross Hospital, Hangzhou 310004, Zhejiang, China

Correspondence Address:
Dr. Xilie Ma
Department of Osteology, Hangzhou Red Cross Hospital, No. 208 Huancheng East Road, Hangzhou 310004, Zhejiang
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0304-4920.360035

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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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