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暴露于BaP/BPDE会导致人体 trofhoblast 细胞功能障碍,并通过上调 lnc-HZ06-调节的 IL1BB,诱导流产

Jiarong Guo¹, Jingsong Zhao², Peng Tian²

¹Key Laboratory of Environment and Female Reproductive Health, The Eighth Affiliated Hospital, Sun Yat-sen University, Shenzhen 518033, China; Key Laboratory of Environment and Female Reproductive Health, West China School of Public Health & West China Fourth Hospital, Sichuan University, Chengdu 610041, China; Chengdu Qingyang District for Disease Control and Prevention, Chengdu 610031, China.

Journal of hazardous materials

|July 11, 2024

概括

对[a]烯 (BaP) 和其代谢物BPDE的环境暴露会通过损害热囊细胞诱导流产. 一种新的lncRNA,lnc-HZ06和IL1B被确定为这个过程中的关键参与者,提供潜在的治疗点.

科学领域:

生殖生物学生殖生物学
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.

背景情况:

[a]烯 (BaP) 和其代谢物BPDE的暴露可能导致热囊细胞功能障碍和流产.
长非编码RNAs (lncRNAs) 参与调节这些过程.
炎症性细胞因子IL1B及其表观遗传调节在BaP/BPDE诱导流产中的作用尚不清楚.

研究的目的:

调查IL1B和一种新型lncRNA,Inc-HZ06在BaP/BPDE诱导的热囊细胞功能障碍和流产中的作用.
阐明由lnc-HZ06.6调节IL1B的表观遗传机制.
探索BaP/BPDE诱导流产的潜在治疗点.

主要方法:

分析BPDE-DNA添加物,热囊细胞功能和流产率.
在暴露细胞,人类流产组织和小鼠模型中量化lnc-HZ06和IL1B的表达.
研究涉及STAT4,METTL3,HuR和TBP的分子机制.
在体内研究中,使用暴露于BaP的小鼠进行Inc-hz06或Il1b敲击.

主要成果:

BPDE-DNA附加物,热囊细胞功能障碍和流产是相关的.
在暴露于BPDE的细胞,反复流产的组织和暴露于BaP的小鼠中,Inc-HZ06和IL1B的上调调节.
无论是lnc-HZ06还是IL1B,都会影响 trofhoblast 细胞的迁移/入侵,并促进细胞亡.
lnc-HZ06通过STAT4介导的转录和METTL3/HuR复合体介导的mRNA稳定性来提高IL1B的调节.
暴露于BPDE会通过TBP增加Inc-HZ06的转录,导致IL1B水平升高.
抑制lnc-hz06或Il1b可以改善小鼠的BaP诱导流产.

结论:

这项研究揭示了涉及lnc-HZ06和IL1B的不明原因流产的新机制.
通过Inc-HZ06介导的IL1B上调调节,BaP/BPDE暴露会诱导热囊细胞功能障碍和流产.
lnc-HZ06和IL1B代表了预防和治疗BaP/BPDE诱导的流产的潜在治疗点.

关键词:

在 BaP 或 BPDE 的情况下.细胞亡,迁移/入侵在Lnc-HZ06和IL1BB.在M6ARNA修饰过程中.71 或 HTR-8/SVneo 细胞无法解释的反复流产

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