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双S通过NR1H3降解扰乱人类状细胞的功能:从集成的批量和单细胞转录组学的机制性见解
Zhongwen Lu1, Peng Xue1, Daoyuan Lu1
1Department of Urology, The Affiliated Lianyungang Hospital of Xuzhou Medical University, The First People's Hospital of Lianyungang, Lianyungang, Jiangsu, China.
Ecotoxicology and environmental safety
|November 16, 2025
概括
双S (BPS) 通过向NR1H3.3,损害人类塞尔托利细胞的功能和增殖. 对BPS毒性的这种分子洞察力可能解释了它对男性不孕症的贡献.
科学领域:
- 生殖生物学 生殖生物学
- 环境毒理学环境毒理学
- 分子内分泌学分子内分泌学
背景情况:
- 男性不孕症是一个越来越令人担忧的问题,其中涉及诸如双S (BPS) 等环境污染物.
- 精确的分子机制,BPS影响人类塞尔托利细胞,精子生成至关重要,并没有完全理解.
研究的目的:
- 阐明人类塞尔托利细胞中BPS诱导的毒性背后的分子机制.
- 确定关键的调控因素和潜在的治疗点,涉及到BPS受损的精子生成.
主要方法:
- 人类塞尔托利细胞暴露在BPS中,评估了活力,增殖和转录基因变化.
- 集成的批量和单细胞RNA测序与计算分析 (药映射,分子对接,模拟) 确定了BPS目标.
- 功能验证涉及NR1H3敲除/过度表达试验,光酶记者和西部斑点.
主要成果:
- 在度≥20μM时,BPS抑制了塞尔托利细胞活力和增殖.
- BPS诱导了影响细胞周期,新陈代谢和类固醇生成的转录组失调.
- NR1H3被确定为直接的BPS标,BPS降低NR1H3水平和活性;NR1H3调制影响了细胞存活率.
结论:
- BPS通过直接向和降低NR1H3.3的调节,损害了人类塞尔托利细胞的功能.
- NR1H3 在塞尔托利细胞存活中起着关键作用.
- BPS诱导的男性不孕症可能通过NR1H3介导的途径发生,突出NR1H3作为潜在的治疗点.
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