MiR-124-3p/EIF3B通过PI3K/AKT信号通路调节由克拉米迪亚虫诱导的宿主细胞亡
Ting Tong1,2, Yunfei Li1, You Zhou1
1Department of public health laboratory sciences, school of public health, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China.
The Journal of infectious diseases
|November 19, 2024
概括
克拉米迪亚虫感染引发了人类支气管上皮细胞通过miR-124-3p向EIF3B的亡. 这种机制激活PI3K/AKT通路,影响疾病的进展.
科学领域:
- 微生物学 微生物学
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
背景情况:
- 克拉米迪亚虫是一种引起人类呼吸系统疾病的动物性病原体.
- 克拉米迪亚感染与亡有关,微RNAs (miRNAs) 中介调节作用.
研究的目的:
- 研究miR-124-3p在人类支气管上皮细胞中C. psittaci诱导的亡中的作用.
- 阐明涉及miR-124-3p,其目标基因EIF3B以及PI3K/AKT信号通路的调节机制.
主要方法:
- 用C. psittaci感染HBE细胞.
- 对亡,miRNA和mRNA表达水平的分析.
- 路西法酶记者测定以确认目标基因相互作用.
- 抑制剂/模仿转染和siRNA淘汰试验.
- 西部涂抹以评估蛋白质表达和通路激活.
主要成果:
- C. psittaci感染诱导了显著的HBE细胞亡和上调的miR-124-3p.
- EIF3B被确定为miR-124-3p的直接标,具有反向表达相关性.
- 抑制miR-124-3p降低了细胞亡和C. psittaci的复制,同时抑制PI3K/AKT.
- miR-124-3p模仿显示出相反的效果,而EIF3B siRNA逆转了miR-124-3p抑制剂的效果.
结论:
- miR-124-3p通过向EIF3B.通过向C. psittaci感染的HBE细胞促进细胞亡.
- 这一miR-124-3p/EIF3B轴激活PI3K/AKT信号通路.
- 这项研究揭示了克拉米迪亚与宿主细胞相互作用中的新型分子机制.
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