LncRNA MALAT1 Promotes Neuronal Apoptosis During Spinal Cord Injury Through miR-199a-5p/ PRDM5 Axis.

IF 0.9 4区医学 Q4 CLINICAL NEUROLOGY Turkish neurosurgery Pub Date : 2024-01-01 DOI:10.5137/1019-5149.JTN.36175-21.5

Xieli Guo, Huan Chen, Suonan Li, Shuai Zhang, Yong Gong, Jiangliu Yin

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Abstract

Aim: To determine the regulation of long non-coding RNA (lncRNA) MALAT1 on neuronal apoptosis during spinal cord injury (SCI) and to explore its possible mechanisms.

Material and methods: The motor ability of SCI rat models and apoptosis in spinal cord tissue were evaluated. Primary spinal cord neurons (SCNs) were isolated and treated with H2O2 before cell transfection. The apoptosis of SCNs and expression of PRDM5 and MALAT1 were also measured. The interactions among MALAT1, miR-199a-5p, and PRDM5 were detected.

Results: The motor ability of SCI rats decreased significantly. The proportion of apoptotic neurons increased in damaged tissue and SCN, along with an increase in the expression of apoptosis-related proteins c-caspase-3/9, autophagy-related proteins (p62 and LC3 II/I ratio), and proinflammatory factors. Moreover, overexpression of MALAT1 and PRDM5 in damaged SCN resulted in an increased apoptosis rate of neurons, elevated expression of apoptosis-related proteins, and upregulated levels of inflammatory factors. However, miR-199a-5p overexpression/PRDM5 knockdown partially counteracted the effects of MALAT1 overexpression on H2O2-induced SCNs. In addition, MALAT1 negatively regulated miR-199a-5p, which targeted PRDM5.

Conclusion: LncRNA MALAT1 promotes neuronal apoptosis during SCI by regulating the miR-199a-5p/PRDM5 axis.

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长非编码 RNA MALAT1 通过 miR-199a-5p/PRDM5 轴促进脊髓损伤过程中的神经细胞凋亡

目的：本研究旨在确定长非编码RNA（lncRNA）MALAT1对脊髓损伤（SCI）过程中神经细胞凋亡的调控作用，并探讨其可能的机制：评估SCI大鼠模型的运动能力和脊髓组织的凋亡。分离原代脊髓神经元（SCNs）并在细胞转染前用 H2O2 处理。同时还测定了脊髓神经元的凋亡以及 PRDM5 和 MALAT1 的表达。结果发现，MALAT1、miR-199a-5p和PRDM5之间存在相互作用：结果：SCI 大鼠的运动能力明显下降。结果：SCI大鼠的运动能力明显下降，受损组织和SCN中凋亡神经元的比例增加，凋亡相关蛋白c-caspase-3/9、自噬相关蛋白（p62和LC3 II/I比值）和促炎因子的表达增加。此外，在受损的 SCN 中过表达 MALAT1 和 PRDM5 会导致神经元凋亡率增加、凋亡相关蛋白表达升高以及炎症因子水平上调。然而，miR-199a-5p 的过表达/PRDM5 的敲除部分抵消了 MALAT1 过表达对 H2O2 诱导的 SCN 的影响。此外，MALAT1 负向调节 miR-199a-5p，而 miR-199a-5p 则靶向 PRDM5：结论：LncRNA MALAT1通过调节miR-199a-5p/PRDM5轴促进SCI过程中神经元的凋亡。

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

Turkish neurosurgery 医学-临床神经学

CiteScore

1.50

自引率

12.50%

发文量

126

审稿时长

2 months

期刊介绍： Turkish Neurosurgery is a peer-reviewed, multidisciplinary, open access and totally free journal directed at an audience of neurosurgery physicians and scientists. The official language of the journal is English. The journal publishes original articles in the form of clinical and basic research. Turkish Neurosurgery will only publish studies that have institutional review board (IRB) approval and have strictly observed an acceptable follow-up period. With the exception of reference presentation, Turkish Neurosurgery requires that all manuscripts be prepared in accordance with the Uniform Requirements for Manuscripts Submitted to Biomedical Journals.