在急性肝损伤中,IL-33通过巨细胞衍生的异位体miR-27b-3p降低肝脏碳素酶1的调节
Ping Gao1, Min Li2, Jingli Lu3
1Wuhan Children's Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Journal of clinical and translational hepatology
|August 14, 2023
概括
在肝损伤中,介质素-33 (IL-33) 信号增加了外体体中的miR-27b-3p,通过抑制Nrf2.2,抑制碳素化酶1 (CES1). 这种途径解释了肝损伤期间CES1的减少.
科学领域:
- 肝病学和免疫学 肝病学和免疫学
- 肝脏损伤的分子机制
- 通过外体介导的细胞通信
背景情况:
- 在肝损伤中,碳氧乙酶1 (CES1) 表达减少.
- 干白素-33 (IL-33) 在肝损伤期间调节CES1的作用尚不清楚.
研究的目的:
- 为了研究IL-33在肝损伤中的功能.
- 阐明IL-33影响CES1表达的机制.
主要方法:
- 在人肝样本和小鼠模型中量化IL-33和CES1 (LPS-,APAP诱导的损伤).
- 产生和分析IL-33和ST2淘汰赛小鼠.
- 使用miR测序识别IL-33响应细胞和对巨细胞衍生的外体 (MDEs) 的表征.
主要成果:
- 患者肝脏中IL-33和CES1水平之间的反相关性;在IL-33/ST2缺乏的小鼠中,CES1下调得到改善.
- 巨细胞调解IL-33效应;IL-33刺激的MDEs降低了肝细胞中CES1的表达.
- 刺激IL-33增加了外体miR-27b-3p,它准了Nrf2;这种调节取决于GATA3.3.
结论:
- 在MDEs中,IL-33-ST2-GATA3通路会提高miR-27b-3p.
- 肝细胞吸收这些外体细胞会通过Nrf2抑制抑制CES1.
- 这项研究阐明了导致肝损伤CES1失调的关键机制.
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