mettl3介导的miR-192-5p成熟靶向ATG7,阻止周围神经损伤中的雪旺细胞自噬。

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC
Xing Liu, Jun Lv, Weilong Tang, Yuanbai Hu, Yiwei Wen, Hongtao Shen
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引用次数: 0

摘要

抑制miR-192-5p可以促进周围神经损伤(PNI)大鼠的神经修复,但这种作用的确切机制尚不清楚。自噬相关基因(ATG)蛋白介导的雪旺细胞(SC)自噬在PNI中起关键作用,但miR-192-5p是否影响SC自噬在PNI中的参与尚不确定。在这项研究中,我们研究了甲基转移酶样蛋白3 (METTL3)/miR-192-5p/ATG7对大鼠PNI模型和SC氧葡萄糖剥夺模型中SC自噬的影响。结果显示,METTL3通过m6A甲基化刺激miR-192-5p成熟,抑制ATG7和SC自噬,加重PNI。这些发现为PNI患者的治疗提供了新的靶点和潜在的基础。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
METTL3-mediated maturation of miR-192-5p targets ATG7 to prevent Schwann cell autophagy in peripheral nerve injury.

The inhibition of miR-192-5p can promote nerve repair in rats with peripheral nerve injury (PNI) but the precise mechanisms underlying this effect remain unclear. Schwann cell (SC) autophagy mediated by autophagy-related gene (ATG) proteins has a key role in PNI but it is uncertain whether miR-192-5p affects the involvement of SC autophagy in PNI. In this study, we investigated the impact of methyltransferase-like protein 3 (METTL3)/miR-192-5p/ATG7 on SC autophagy in a rat PNI model and in an SC oxygen and glucose deprivation model. The results revealed that METTL3 stimulated miR-192-5p maturation via m6A methylation to depress ATG7 and SC autophagy and aggravate PNI. These findings provide a new target and potential basis for the treatment of patients with PNI.

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CiteScore
7.20
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4.30%
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