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在小鼠中,miR-144-3p抑制通过发育性暴露诱导的Nrf2激活

Ruirui Wu¹, Xin Chen¹, Yongqin Xia¹

¹Key Laboratory of Environmental Stress and Chronic Disease Control & Prevention Ministry of Education (China Medical University), Shenyang, Liaoning 110122, China; Key Laboratory of Liaoning Province on Toxic and Biological Effects of Arsenic (China Medical University), Shenyang, Liaoning, China; School of Public Health, China Medical University, Shenyang, Liaoning, China.

|July 2, 2025

概括

发育期的暴露会激活肝脏核因素与红色素2相关的因子2 (Nrf2) 在幼中,增加肝脏疾病的风险. 这种激活是通过抑制microRNA-144-3p (miR-144-3p) 来实现的.

科学领域:

环境毒理学环境毒理学
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
分子生物学分子生物学

背景情况:

在发育过程中接触会增加肝脏疾病的风险,这与核因素红色素2相关因子2 (Nrf2) 激活有关.
表观遗传机制与Nrf2激活有关,但确切的途径尚不清楚.

研究的目的:

研究开发性暴露激活肝脏Nrf2的机制.
探索微RNAs (miRNAs) 在调解诱导的Nrf2激活中的作用.

主要方法:

评估了暴露于的断奶幼中的Nrf2活性及其下游基因表达.
测量了全球DNA甲基化和Nrf2促进体甲基化.
量化了肝脏中的miRNA水平 (miR-144-3p,miR-27a-3p,miR-101a-3p,miR-155-5p).
利用初级小鼠肝细胞来测试miR-144-3p抑制对Nrf2及其向基因的影响.

主要成果:

在幼中,暴露 (0.5 ppm) 增加了肝脏Nrf2活性 (1.5倍) 和血液GSH/GSSG比率 (4.4倍).
DNA甲基化水平没有显著改变.
miR-144-3p和miR-27a-3p的水平下降,而miR-101a-3p和miR-155-5p的水平增加.
在肝细胞中抑制miR-144-3p可上调Nrf2及其向基因 (Gclc,Gclm,Gsr).

结论:

发育期的暴露会在断奶后的幼中激活肝脏Nrf2.
诱导的Nrf2激活是通过抑制miR-144-3p进行的.
这些发现阐明了一种新的表观遗传机制,将发育期暴露与肝病风险增加联系起来.

关键词:

亚是一种.通过DNA甲基化.发展性的发展.Nrf2 没有任何问题.这是一个小RNARNA.

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