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miR-129-5p 通过与 SIAH1 结合并激活 mTOR 信号通路来减轻缺血性脑损伤。

miR-129-5p Ameliorates Ischemic Brain Injury by Binding to SIAH1 and Activating the mTOR Signaling Pathway.

机构信息

Department of Critical Care Medicine, The First Hospital of Jilin University, Changchun, 130000, P. R. China.

出版信息

J Mol Neurosci. 2021 Sep;71(9):1761-1771. doi: 10.1007/s12031-021-01872-0. Epub 2021 Aug 5.

Abstract

Aberrant expression of microRNAs (miRNAs) has been linked with ischemic brain injury (IBI), but the mechanistic actions behind the associated miRNAs remain to be determined. Of note, miR-129-5p was revealed to be downregulated in the serum of patients with IBI. In silico prediction identified a putative target gene, siah E3 ubiquitin protein ligase 1 (SIAH1), of miR-129-5p. Accordingly, this study plans to clarify the functional relevance of the interplay of miR-129-5p and SIAH1 in IBI. IBI was modeled by exposing human hippocampal neuronal cells to oxygen-glucose deprivation (OGD) in vitro and by occluding the middle cerebral artery (MCAO) in a mouse model in vivo. Apoptosis of hippocampal neuronal cells was assessed by annexin V-FITC/PI staining and TUNEL staining. The area of cerebral infarction was measured using TTC staining, along with neurological scoring on modeled mice. Loss of hippocampal neuronal cells in the peri-infarct area was monitored using Nissl staining. Downregulated miR-129-5p expression was found in OGD-induced hippocampal neuronal cells and MCAO-treated mice. Mechanistically, miR-129-5p was validated to target and inhibit SIAH1 through the application of dual-luciferase reporter assay. Additionally, enforced miR-129-5p inhibited the apoptosis of OGD-induced cells and decreased the cerebral infarct area, neurological scores and apoptosis of hippocampal neuronal cells by downregulating SIAH1 and activating the mTOR signaling pathway. Taken together, the results of this study reveal the important role and underlying mechanism of miR-129-5p in IBI, providing a promising biomarker for preventive and therapeutic strategies.

摘要

异常表达的 microRNAs(miRNAs)与缺血性脑损伤(IBI)有关,但相关 miRNAs 的作用机制仍有待确定。值得注意的是,miR-129-5p 在 IBI 患者的血清中表达下调。通过计算机预测,确定了 miR-129-5p 的一个潜在靶基因,即 SIAH1。因此,本研究计划阐明 miR-129-5p 与 SIAH1 相互作用在 IBI 中的功能相关性。通过体外氧葡萄糖剥夺(OGD)处理人海马神经元细胞和体内大脑中动脉闭塞(MCAO)建立 IBI 模型。通过 Annexin V-FITC/PI 染色和 TUNEL 染色评估海马神经元细胞的凋亡。通过 TTC 染色和对模型小鼠进行神经学评分来测量脑梗死面积。通过尼氏染色监测梗死周围区海马神经元细胞的丢失。OGD 诱导的海马神经元细胞和 MCAO 处理的小鼠中发现 miR-129-5p 表达下调。通过双荧光素酶报告基因检测验证了 miR-129-5p 通过靶向和抑制 SIAH1 发挥作用。此外,过表达 miR-129-5p 通过下调 SIAH1 并激活 mTOR 信号通路抑制 OGD 诱导的细胞凋亡,减少脑梗死面积、神经学评分和海马神经元细胞凋亡。总之,本研究结果揭示了 miR-129-5p 在 IBI 中的重要作用和潜在机制,为预防和治疗策略提供了有前途的生物标志物。

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