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 3.2 3区 医学 Q2 CLINICAL NEUROLOGY Journal of Neuropathology and Experimental Neurology Pub Date : 2023-11-20 DOI:10.1093/jnen/nlad091
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。
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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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来源期刊
CiteScore
5.40
自引率
6.20%
发文量
118
审稿时长
6-12 weeks
期刊介绍: Journal of Neuropathology & Experimental Neurology is the official journal of the American Association of Neuropathologists, Inc. (AANP). The journal publishes peer-reviewed studies on neuropathology and experimental neuroscience, book reviews, letters, and Association news, covering a broad spectrum of fields in basic neuroscience with an emphasis on human neurological diseases. It is written by and for neuropathologists, neurologists, neurosurgeons, pathologists, psychiatrists, and basic neuroscientists from around the world. Publication has been continuous since 1942.
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