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介素-17A刺激会诱导微质微RNA表达特征的改变

Yukako Iitani¹, Rika Miki², Kenji Imai¹

¹Department of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, Nagoya, Aichi, 466‑8550, Japan.

Pediatric research

|September 27, 2023

概括

孕产妇免疫激活 (MIA) 涉及中白素-17A (IL-17A) 和微质细胞. 这项研究表明,IL-17A在微质中调节微RNA-206 (miR-206),可能影响神经发育障碍.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
遗传学是一个遗传学.

背景情况:

母亲免疫激活 (MIA) 与后代的神经发育障碍有关.
干白素-17A (IL-17A) 和激活的微质是MIA病理学的关键因素.
对于IL-17A对微质细胞的精确下游影响仍然不完全理解.

研究的目的:

研究IL-17A对微质微RNA (miRNA) 概况的影响.
为了识别微质中由IL-17A调节的特定miRNAs.
在MIA的背景下探索IL-17A诱导的miRNA变化的功能后果.

主要方法:

主要微质细胞被IL-17A刺激,并使用测序和qRT-PCR分析miRNA表达特征.
生物信息学确定了差异表达的miRNAs的目标基因.
向基因表达被验证在微质中感染了miRNA模仿物以及在脂多糖 (LPS) 诱导的MIA小鼠模型中.

主要成果:

激发IL-17A可提高初级微质中的mmu-miR-206-3p表达的调节.
由IL-17A诱导的mumu-miR-206-3p的上调导致其向基因Hdac4和Igf1.1的表达减少.
在MIA小鼠模型的胎儿大脑中,Hdac4的表达也显著降低.

结论:

IL-17A调节微质miRNA配置文件,特别是调节mumu-miR-206-3p.
IL-17A/mmu-miR-206-3p通路影响了神经发育障碍中涉及的基因的表达.
针对这种途径提供了预测和干预MIA相关神经发育缺陷的潜力,包括自闭症谱系障碍 (ASD).

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