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GABARAPL1对于小鼠莱迪格细胞的ACR诱导的自细胞死亡至关重要

Jiahui Meng¹, Linlin Xu², Bingchun Ma¹

¹Department of Physiology, School of Basic Medical Sciences, Jiangxi Medical College, Nanchang University, Nanchang 330006, PR China.

Ecotoxicology and environmental safety

|December 3, 2024

概括

烯胺暴露会通过诱导小鼠莱迪格细胞中的氧化应激和自而导致男性生殖损害. GABARAPL1被确定为这个过程中的关键调解者,由CREB1和PATZ1转录因子调节.

科学领域:

毒理学毒理学毒理学
生殖生物学生殖生物学
细胞生物学细胞生物学

背景情况:

烯胺 (ACR) 是一种工业和食品加工化学物质,已知对男性生殖系统有不良影响.
在ACR诱导的男性生殖毒性的基础上,精确的分子机制在很大程度上是未知的.
氧化应激和自与各种细胞功能障碍有关,包括生殖毒性.

研究的目的:

阐明烯胺损害男性生殖功能的机制.
研究GABAA受体相关蛋白-1 (GABARAPL1) 在ACR诱导对小鼠莱迪格细胞的影响中的作用.
为了确定参与ACR诱导的自的调节因素.

主要方法:

在暴露于ACR的老鼠莱迪格细胞中评估氧化应激和自标志物.
通过过度表达和淘汰研究分析GABARAPL1表达及其功能作用.
通过使用促进物相互作用试验,通过转录因子CREB1和PATZ1对Gabarapl1基因的转录调节的研究.
检查CREB1和PATZ1.1之间的相互作用.

主要成果:

烯胺暴露显著诱导了小鼠莱迪格细胞中的氧化应激和自.
GABARAPL1的表达由ACR上调,在调解ACR诱导的自中起着至关重要的作用.
过度表达GABARAPL1促进了自,而其敲击减弱了ACR诱导的自反应.
转录因子CREB1和PATZ1通过促进因子相互作用协同调节Gabarapl1基因转录,促进ACR诱导的自.
观察到PATZ1和CREB1之间的相互监管关系.

结论:

GABARAPL1是小鼠莱迪格细胞中烯胺诱导的自的关键调解者.
这些发现强调了氧化应激,自和GABARAPL1/CREB1/PATZ1通路在烯胺男性生殖毒性的参与.
这项研究为ACR诱导的男性生殖功能障碍的分子机制提供了新的见解.

关键词:

烯胺是什么烯胺是什么自自是一种自的过程.盖巴拉普尔1的第一名莱迪格细胞是莱迪格细胞.

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