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DDIT4对于DINP诱导的卵巢颗粒细胞自是必不可少的

Yijing Wang¹, Si Yang², Chaoju Hao³

¹Department of Pathology, The First Affiliated Hospital of Nanchang University, Nanchang 330006, PR China; Department of Physiology, School of Basic Medical Sciences, Nanchang University, Nanchang 330006, PR China.

Ecotoxicology and environmental safety

|November 17, 2023

概括

双异尼尔甲酸盐 (DINP) 通过ATF4/DDIT4通路触发卵巢颗粒细胞自. 这项研究阐明了DINP诱导的细胞变化背后的机制,提供了对其生殖毒性的见解.

科学领域:

生殖毒理学生殖毒理学
细胞生物学细胞生物学
内分泌学在内分泌学.

背景情况:

双异尼尔甲酸 (DINP) 是一种广泛使用的可塑化剂,已知对卵巢细胞有影响.
以前的研究表明,DINP在卵巢颗粒细胞中诱导了自,但该机制仍然未知.

研究的目的:

阐明DINP在卵巢颗粒细胞中诱导自的分子机制.
研究DDIT4和ATF4在DINP介导的自中所起的作用.

主要方法:

卵巢颗粒细胞 (KGN细胞) 暴露于DINP.
对DDIT4和ATF4mRNA和蛋白质水平的分析.
对DDIT4和ATF4的基因过度表达和淘汰实验.
染色体免疫沉 (ChIP) 试验以确认转录因子结合.

主要成果:

暴露于DINP会增加DDIT4的表达,并诱导KGN细胞的自.
过度表达DDIT4促进了自,而DDIT4倒置抑制了DINP诱导的自.
ATF4表达被DINP上调调节,并调节了DDIT4转录.
ATF4直接与DDIT4促进区结合.
通过ATF4敲击减弱DINP诱导的DDIT4上调和自.

结论:

通过激活ATF4/DDIT4信号通路,DINP会诱导卵巢颗粒细胞的自.
ATF4/DDIT4轴是DINP对卵巢细胞影响的关键调解器.
了解这种机制对于评估与DINP暴露相关的生殖风险至关重要.

关键词:

在ATF4中使用ATF4.自自是一种自的过程.在DDIT4中,DDIT4是DDIT4.在 DINP 找 DINP 卵巢颗粒细胞是卵巢的颗粒细胞.

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