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miR-463-3p 通过对 SPRR1A 的转录后抑制抑制胫神经再生。

MiR-463-3p inhibits tibial nerve regeneration via post-transcriptional suppression of SPRR1A.

机构信息

Department of Neurology, Huaihe Hospital of Henan University , Kaifeng , China.

出版信息

Artif Cells Nanomed Biotechnol. 2019 Dec;47(1):3631-3637. doi: 10.1080/21691401.2019.1657874.

DOI:10.1080/21691401.2019.1657874
PMID:31468997
Abstract

miRNAs have been involved in neural development, degeneration, and regeneration. MiR-463-3p is expressed in reproductive and nervous systems. In this study, the role of miR-463-3p in tibial nerve injury and regeneration was explored. A model of tibial nerve injury was established with the crush method, and the levels of miR-463-3p were detected at days 0, 3, 7, 12, 18 and 24 post-injury. Then, primary tibial nerve cells were isolated from newborn mice, and miR-463-3p was respectively overexpressed and knocked down in cultured cells. Behaviors of tibial nerve cells were detected. Furthermore, bioinformatics technology was used to investigate the underlying mechanism. The expression miR-463-3p was robustly increased in the injured tibial nerve and in tibial nerve cells treated with oxygen-glucose deprivation. The data on gain- and loss-of-function demonstrated that miR-463-3p negatively regulated including neurite length, percentage of cells with neurites, and cell branching in tibial nerve cells. Small proline-rich repeat protein 1 A (SPRR1A), an identified nerve regeneration associated genes, was identified as a target gene of miR-463-3p. Inhibition of miR-463-3p could increase SPRR1A expression in the tibial nerve tissue and improve regeneration of the tibial nerve post-injury .

摘要

miRNAs 参与神经发育、变性和再生。miR-463-3p 在生殖和神经系统中表达。本研究探讨了 miR-463-3p 在胫骨神经损伤和再生中的作用。采用挤压法建立胫骨神经损伤模型,检测损伤后 0、3、7、12、18 和 24 天 miR-463-3p 水平。然后,从小鼠新生期分离出初级胫骨神经细胞,分别在培养细胞中过表达和敲低 miR-463-3p。检测胫骨神经细胞的行为。此外,还利用生物信息学技术研究其潜在机制。miR-463-3p 在损伤的胫骨神经和氧葡萄糖剥夺处理的胫骨神经细胞中表达明显增加。功能获得和功能丧失的数据表明,miR-463-3p 负调控包括神经突长度、有神经突的细胞百分比和胫骨神经细胞的分支。小脯氨酸丰富重复蛋白 1A(SPRR1A)是鉴定出的与神经再生相关的基因,被鉴定为 miR-463-3p 的靶基因。抑制 miR-463-3p 可增加损伤后胫骨神经组织中 SPRR1A 的表达,改善胫骨神经的再生。

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