在miR-125a-5p/IRF4轴中介于甲诱导的M2巨细胞极化
Yan Yu1,2, Fan Yao1,2, Suyuan Tong1,2
1Key Laboratory of Environmental Stress and Chronic Disease Control and Prevention, Ministry of Education, China Medical University, Shenyang 110122, China.
Biomolecules
|November 27, 2025
概括
暴露将巨细胞转移到M2极化状态,促进瘤生长. 这通过miR-125a-5p/IRF4通路发生,为引起的免疫功能障碍提供了潜在的治疗标.
科学领域:
- 环境毒理学环境毒理学
- 免疫学 免疫学 免疫学
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
背景情况:
- 暴露与包括癌症在内的各种健康问题有关.
- 巨细胞两极分化在免疫反应和瘤发生中起着至关重要的作用.
- 微RNA,如miR-125a-5p在诱导的巨细胞极化中的作用在很大程度上是未知的.
研究的目的:
- 为了研究酸 (NaAsO2) 诱导的巨细胞极化机制.
- 探索miR-125a-5p在这个过程中的作用.
- 为了确定与相关的免疫功能障碍的潜在治疗点.
主要方法:
- 在体内研究中,使用暴露于甲 (NaAsO2) 的老鼠进行了体内研究.
- 在体外研究中,使用与NaAsO2.2治疗的THP-1衍生巨细胞进行了实验.
- 对巨细胞极化标记物 (M1/M2) 和miR-125a-5p表达的分析.
- 研究了miR-125a-5p和干扰素调节因子4 (IRF4) 之间的相互作用.
主要成果:
- 暴露于酸 (NaAsO2) 在体内和体外都诱导了M2巨细胞的极化.
- NaAsO2抑制了miR-125a-5p的表达,并上调了IRF4.
- 过度表达miR-125a-5p可以通过抑制IRF4.4来逆转NaAsO2诱导的M2极化.
结论:
- NaAsO2通过miR-125a-5p/IRF4表观遗传轴促进M2巨细胞的两极分化.
- 这种机制有助于与相关的瘤微环境和免疫功能障碍.
- 向miR-125a-5p为毒性提供了一个潜在的治疗策略.
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