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首页> 外文期刊>FEBS Open Bio >Overexpression of lncRNA TCTN2 protects neurons from apoptosis by enhancing cell autophagy in spinal cord injury
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Overexpression of lncRNA TCTN2 protects neurons from apoptosis by enhancing cell autophagy in spinal cord injury

机译：lncRNA TCTN2的过表达通过增强脊髓损伤中的细胞自噬保护神经元免于凋亡

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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.
机译：神经元凋亡是脊髓损伤（SCI）的主要病理特征，而自噬则通过抑制细胞凋亡来改善神经元损伤。在这里，我们研究了构造家族成员2（TCTN2）长的非编码RNA对SCI细胞凋亡和自噬的作用。 TCTN2在SCI大鼠模型的脊髓组织和氧葡萄糖剥夺诱导的低氧SY-SH-5Y细胞中被下调，而microRNA-216b（miR-216b）被上调。 TCTN2的过表达通过诱导自噬减少神经元的凋亡，并且观察到TCTN2对miR-216b具有负调节作用。此外，TCTN2促进自噬以通过miR-216b-Beclin-1途径抑制凋亡，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途径来增强自噬，从而改善神经元凋亡并减轻脊髓损伤。

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