JunB在二氧化纳米粒子诱导的肺纤维化中协调了巨细胞-纤维细胞交叉
Fei Li1, Dandan Song2, Jiahua Meng3
1Hebei Province Key Laboratory of Occupational Health and Safety for Coal Industry, Hebei Coordinated Innovation Center of Occupational Health and Safety, School of Public Health, North China University of Science and Technology, Tangshan, Hebei 063210, China; Clinical Medical Research Center for Women and Children Diseases, Key Laboratory of Maternal & Fetal Medicine of National Health Commission of China, Shandong Provincial Maternal and Child Health Care Hospital Affiliated to Qingdao University, Jinan 250014, China.
Ecotoxicology and environmental safety
|September 13, 2025
概括
暴露于纳米粒子会通过激活JunB信号来引起肺纤维化. 用T-5224抑制JunB为治疗这种职业危险提供了一个有希望的治疗策略.
科学领域:
- 环境健康 环境健康
- 毒理学 毒理学 毒理学
- 分子生物学分子生物学
背景情况:
- 纳米粒子 (SiNP) 暴露是一种已知的职业和环境危害,导致肺纤维化.
- 驱动SiNP诱导的肺纤维化的精确分子途径尚未完全理解.
研究的目的:
- 调查JunB信号在纳米粒子诱导的肺纤维化中的作用.
- 评估针对JunB.的治疗潜力.
主要方法:
- 使用了体外巨细胞纤维细胞共同培养和体内小鼠模型.
- 通过药理抑制 (T-5224) 和遗传沉默来研究JunB的功能.
- RNA测序确定了基因表达变化和调节途径.
主要成果:
- SiNPs诱导了巨细胞灭,通过JunB/AP-1通路激活导致纤维细胞转基因分化.
- 在体外,JunB沉默和T-5224治疗抑制了纤维细胞转差.
- 在暴露于SiNP的小鼠中,T-5224的使用减少了原沉积和纤维化标志物.
结论:
- JunB是二氧化纳米颗粒诱导的肺纤维化中的关键媒介.
- 药理上抑制JunB证明了肺纤维化治疗的治疗潜力.
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