MiR-30b-5p alleviates trigeminal neuralgia induced by chronic constriction injury of the infraorbital nerve by regulating the voltage-gated sodium channel Nav1.3 in rats

IF 2.5 4区 医学 Q3 NEUROSCIENCES
Tingting Hu , Mengci Shao , Jiajia Liu , Xiaorong Yan , Liecheng Wang , Yuanyin Wang , Wenhua Xu
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引用次数: 0

Abstract

Nav1.3 is a tetrodotoxin-sensitive voltage-gated sodium channel isoform encoded by SCN3A, the abnormal expression of which plays a crucial role in the generation of ectopic discharge, as well as being associated with allodynia and hyperalgesia. Using bioinformatics analysis, we showed that miR-30b-5p directly targets SCN3A. We aimed to explore whether miR-30b-5p can participate in trigeminal neuralgia (TN) in rats by regulating the expression of Nav1.3. The rat TN model was constructed through infraorbital nerve-chronic constriction injury (ION-CCI), which was verified by measuring the change in mechanical threshold and the expression of activating transcription factor 3 (a marker of nerve damage) in the trigeminal ganglia (TG). The expression of miR-30b-5p in postoperative TG was downregulated, whereas that of Nav1.3 was upregulated in rats subjected to ION-CCI. Overexpression of miR-30b-5p repressed the expression of Nav1.3 in TG and alleviated ION-CCI-induced TN. MiR-30b-5p targets to regulate the expression of SCN3A, thereby reducing or aggravating TN. Therefore, miR-30b-5p may be a novel therapeutic target for neuropathic pain.
MiR-30b-5p通过调节电压门控钠通道Nav1.3减轻大鼠眶下神经慢性收缩损伤所致三叉神经痛。
Nav1.3是一种由SCN3A编码的河豚毒素敏感电压门控钠通道异构体,其异常表达在异位放电的产生中起着至关重要的作用,并与异位性疼痛和痛觉过敏有关。通过生物信息学分析,我们发现miR-30b-5p直接靶向SCN3A。我们旨在探讨miR-30b-5p是否通过调节Nav1.3的表达参与大鼠三叉神经痛(TN)的发生。通过眶下神经慢性收缩损伤(ION-CCI)构建大鼠TN模型,通过测量三叉神经节(TG)机械阈值变化和神经损伤标志物激活转录因子3的表达进行验证。离子- cci大鼠术后TG中miR-30b-5p表达下调,而Nav1.3表达上调。过表达miR-30b-5p可抑制TG中Nav1.3的表达,减轻离子cci诱导的TN。miR-30b-5p可调控SCN3A的表达,从而减轻或加重TN。因此,miR-30b-5p可能是神经性疼痛的新治疗靶点。
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来源期刊
Neuroscience Letters
Neuroscience Letters 医学-神经科学
CiteScore
5.20
自引率
0.00%
发文量
408
审稿时长
50 days
期刊介绍: Neuroscience Letters is devoted to the rapid publication of short, high-quality papers of interest to the broad community of neuroscientists. Only papers which will make a significant addition to the literature in the field will be published. Papers in all areas of neuroscience - molecular, cellular, developmental, systems, behavioral and cognitive, as well as computational - will be considered for publication. Submission of laboratory investigations that shed light on disease mechanisms is encouraged. Special Issues, edited by Guest Editors to cover new and rapidly-moving areas, will include invited mini-reviews. Occasional mini-reviews in especially timely areas will be considered for publication, without invitation, outside of Special Issues; these un-solicited mini-reviews can be submitted without invitation but must be of very high quality. Clinical studies will also be published if they provide new information about organization or actions of the nervous system, or provide new insights into the neurobiology of disease. NSL does not publish case reports.
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