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环境 BaP/BPDE 抑制了 trofhoblast 细胞的入侵/迁移,并通过下调 lnc-HZ01/MEST/VIM 轴诱导流产

Weina Chen¹, Yuanlv Deng², Yan Li³

¹Research Center for Environment and Female Reproductive Health, the Eighth Affiliated Hospital, Sun Yat-sen University, Shenzhen 518033, China.

Ecotoxicology and environmental safety

|May 3, 2024

概括

对甲 (BaP) 和其代谢物BPDE的环境暴露可以通过抑制热囊细胞入侵而导致流产. 这项研究揭示了涉及lnc-HZ01和MEST/VIM通路的机制,为生殖毒性提供了洞察力.

科学领域:

生殖毒理学生殖毒理学
内分泌学在内分泌学.
分子生物学分子生物学

背景情况:

甲 (BaP) 和其代谢物BPDE是与流产相关的内分泌干扰化学物质.
导致BAP/BPDE流产的精确分子机制在很大程度上是未知的.

研究的目的:

阐明BPDE抑制 trofhoblast细胞入侵和迁移的分子机制.
研究Inc-HZ01和MEST/VIM通路在BPDE诱导流产中的作用.
为了验证人类反复流产 (RM) 组织和BAP暴露的小鼠模型中的发现.

主要方法:

人类热细胞 (天71) 暴露于BPDE.
细胞入侵和迁移试验的分析.
对基因表达进行定量实时PCR (qRT-PCR) (lnc-HZ01,MEST,VIM).
使用暴露于BaP的小鼠进行体内研究.

主要成果:

通过抑制MEST/VIM通路,BPDE暴露抑制了热囊细胞的入侵/迁移.
BPDE增加了Inc-HZ01的表达,这进一步抑制了MEST/VIM通路和细胞入侵/迁移.
抑制lnc-HZ01或过度表达的MEST救出了BPDE诱导的细胞入侵/迁移的影响.
与健康对照人相比,lnc-HZ01在人体RM小组织中受到上调,MEST/VIM在人体RM小组织中受到下调.
暴露于BaP抑制了小鼠Mest/Vim通路,并在小鼠中诱导流产.

结论:

暴露于BaP/BPDE会通过lnc-HZ01/MEST/VIM通路抑制热囊细胞的入侵/迁移,从而导致流产.
这种机制在人体热囊细胞,人体RM组织和小鼠模型中得到保护.
这些发现为BaP/BPDE对女性生殖的毒理风险提供了新的见解.

关键词:

环境BaP/BPDE环境BaP/BPDE环境 MEST/以及入侵/迁移.流产流产流产没有编码的RNA lnc-HZ01 热囊细胞天71细胞

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