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miR-342-5p针对CTNNBIP1促进肠道病毒71的复制

Chengyan Tang¹, Yu Chen², Hongjiao Jin²

¹Suzhou Medical College of Soochow University, Suzhou, 215123, People's Republic of China; Department of Pediatric Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, People's Republic of China; Department of Pediatric Surgery, Guizhou Children's Hospital, Zunyi, 563000, People's Republic of China.

Microbial pathogenesis

|July 21, 2023

概括

微RNA miR-342-5p促进了肠道病毒71 (EV71) 的复制,并损害了先天免疫反应. 这通过准CTNNBIP1,影响Wnt/CTNNB1信号通路和I型干扰素的产生来实现.

科学领域:

病毒学病毒学
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

肠道病毒71 (EV71) 是一个重要的人类病原体,导致严重的神经疾病.
越来越多地认识到微RNA (miRNA) 在病毒复制和宿主免疫反应中的作用.
miR-342-5p已涉及到各种细胞过程,但其在EV71感染中的特定功能需要阐明.

研究的目的:

调查miR-342-5p在71 Enterovirus (EV71) 复制中的作用.
阐明 miR-342-5p 影响 EV71 感染和宿主免疫反应的潜在分子机制.

主要方法:

在哺乳小鼠和HMC3细胞中感染EV71.
转录组测序用于差异基因和miRNA分析.
双 luciferase 记者测定以确认目标基因结合.
细胞活力测定 (CCK-8).
分子测定包括RT-qPCR,西斑,免疫光和免疫组织化学,以评估病毒蛋白水平和炎症标志物.

主要成果:

转录组分析揭示了Wnt通路的参与,并确定CTNNBIP1作为miR-342-5p.p.的目标.
过度表达miR-342-5p显著促进了EV71 VP1 mRNA和细胞和小鼠脊髓组织中的蛋白质表达.
miR-342-5p的过度表达增加了促炎性细胞因子 (TNF-α,IL-6,IL-10) 和抑制的抗病毒干扰素-β (IFN-β) 水平.
高表达的miR-342-5p破坏了神经元结构,并减少了质细胞数量.
过度表达的CTNNBIP1抵消了miR-342-5p的影响,减少了病毒复制和调节细胞因子配置.
该机制涉及miR-342-5p针对CTNNBIP1,抑制其表达,并随后增强Wnt/CTNNB1/TCF4相互作用,导致改变I型干扰素反应.

结论:

miR-342-5p作为神经细胞和组织中EV71复制的积极调节剂.
过度表达miR-342-5p通过Wnt/CTNNB1信号通路减弱了先天的抗病毒免疫反应.
向miR-342-5p或调节Wnt通路可能提供针对EV71感染的治疗策略.

关键词:

肠道病毒 71 病毒.脚病是口病的一种疾病.手手手的手的手.病毒复制是病毒的复制.没有信号通路.在 miR-342-5p 中.

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