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长链非编码 RNA TCTN2 的过表达通过增强细胞自噬来保护脊髓损伤中的神经元免于凋亡。

Overexpression of lncRNA TCTN2 protects neurons from apoptosis by enhancing cell autophagy in spinal cord injury.

机构信息

Department of Rehabilitation, The General Hospital, Tianjin Medical University, China.

出版信息

FEBS Open Bio. 2019 Jul;9(7):1223-1231. doi: 10.1002/2211-5463.12651. Epub 2019 Jun 4.

DOI:10.1002/2211-5463.12651
PMID:31050183
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6609579/
Abstract

Neuronal apoptosis is the main pathological feature of spinal cord injury (SCI), while autophagy contributes to ameliorating neuronal damage via inhibition of apoptosis. Here, we investigated the role of tectonic family member 2 (TCTN2) long non-coding RNA on apoptosis and autophagy in SCI. TCTN2 was down-regulated in the spinal cord tissues of a rat model of SCI and in oxygen-glucose deprivation-induced hypoxic SY-SH-5Y cells, while microRNA-216b (miR-216b) was up-regulated. Overexpression of TCTN2 reduced neuron apoptosis by inducing autophagy, and TCTN2 was observed to negatively regulate miR-216b. Furthermore, TCTN2 promoted autophagy to repress apoptosis through the miR-216b-Beclin-1 pathway, and overexpression of TCTN2 improved neurological function in the SCI rat model. In summary, our data suggest that TCTN2 enhances autophagy by targeting the miR-216b-Beclin-1 pathway, thereby ameliorating neuronal apoptosis and relieving spinal cord injury.

摘要

神经元凋亡是脊髓损伤 (SCI) 的主要病理特征,而自噬通过抑制细胞凋亡有助于减轻神经元损伤。在这里,我们研究了结构域家族成员 2 (TCTN2) 长非编码 RNA 在 SCI 中对细胞凋亡和自噬的作用。在 SCI 大鼠模型和氧葡萄糖剥夺诱导的缺氧 SY-SH-5Y 细胞中,TCTN2 表达下调,而 microRNA-216b (miR-216b) 表达上调。TCTN2 的过表达通过诱导自噬减少神经元凋亡,并且观察到 TCTN2 负调控 miR-216b。此外,TCTN2 通过 miR-216b-Beclin-1 通路促进自噬来抑制细胞凋亡,并且 TCTN2 的过表达改善了 SCI 大鼠模型的神经功能。总之,我们的数据表明,TCTN2 通过靶向 miR-216b-Beclin-1 通路增强自噬,从而减轻神经元凋亡并缓解脊髓损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fb4/6609579/52d5d3d20a72/FEB4-9-1223-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fb4/6609579/03398914bb52/FEB4-9-1223-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fb4/6609579/49e8ab04c53f/FEB4-9-1223-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fb4/6609579/9b710ada1a44/FEB4-9-1223-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fb4/6609579/52d5d3d20a72/FEB4-9-1223-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fb4/6609579/03398914bb52/FEB4-9-1223-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fb4/6609579/3c143a1f13a6/FEB4-9-1223-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fb4/6609579/49e8ab04c53f/FEB4-9-1223-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fb4/6609579/9b710ada1a44/FEB4-9-1223-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fb4/6609579/52d5d3d20a72/FEB4-9-1223-g005.jpg

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