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

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 wa...

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Main Authors: Xiao‐dong Ren, Chun‐xiao Wan, Ya‐li Niu
Format: Article
Language:English
Published: Wiley 2019-07-01
Series:FEBS Open Bio
Subjects:
Online Access:https://doi.org/10.1002/2211-5463.12651
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spelling doaj-621b71e8971c48b4a63f03cb53b5c0b32020-11-25T03:24:50ZengWileyFEBS Open Bio2211-54632019-07-01971223123110.1002/2211-5463.12651Overexpression of lncRNA TCTN2 protects neurons from apoptosis by enhancing cell autophagy in spinal cord injuryXiao‐dong Ren0Chun‐xiao Wan1Ya‐li Niu2Department of Rehabilitation The General Hospital Tianjin Medical University ChinaDepartment of Rehabilitation The General Hospital Tianjin Medical University ChinaDepartment of Rehabilitation The General Hospital Tianjin Medical University ChinaNeuronal 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.https://doi.org/10.1002/2211-5463.12651autophagyBeclin‐1miR‐216bneuronal apoptosisspinal cord injuryTCTN2
collection DOAJ
language English
format Article
sources DOAJ
author Xiao‐dong Ren
Chun‐xiao Wan
Ya‐li Niu
spellingShingle Xiao‐dong Ren
Chun‐xiao Wan
Ya‐li Niu
Overexpression of lncRNA TCTN2 protects neurons from apoptosis by enhancing cell autophagy in spinal cord injury
FEBS Open Bio
autophagy
Beclin‐1
miR‐216b
neuronal apoptosis
spinal cord injury
TCTN2
author_facet Xiao‐dong Ren
Chun‐xiao Wan
Ya‐li Niu
author_sort Xiao‐dong Ren
title Overexpression of lncRNA TCTN2 protects neurons from apoptosis by enhancing cell autophagy in spinal cord injury
title_short Overexpression of lncRNA TCTN2 protects neurons from apoptosis by enhancing cell autophagy in spinal cord injury
title_full Overexpression of lncRNA TCTN2 protects neurons from apoptosis by enhancing cell autophagy in spinal cord injury
title_fullStr Overexpression of lncRNA TCTN2 protects neurons from apoptosis by enhancing cell autophagy in spinal cord injury
title_full_unstemmed Overexpression of lncRNA TCTN2 protects neurons from apoptosis by enhancing cell autophagy in spinal cord injury
title_sort overexpression of lncrna tctn2 protects neurons from apoptosis by enhancing cell autophagy in spinal cord injury
publisher Wiley
series FEBS Open Bio
issn 2211-5463
publishDate 2019-07-01
description 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.
topic autophagy
Beclin‐1
miR‐216b
neuronal apoptosis
spinal cord injury
TCTN2
url https://doi.org/10.1002/2211-5463.12651
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AT chunxiaowan overexpressionoflncrnatctn2protectsneuronsfromapoptosisbyenhancingcellautophagyinspinalcordinjury
AT yaliniu overexpressionoflncrnatctn2protectsneuronsfromapoptosisbyenhancingcellautophagyinspinalcordinjury
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