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ATF6是精子细胞中介导的亡的关键调节者

Sung Woo Lee^1,2, Bokyung Kim², Jung Bae Seong³

¹School of Life Sciences, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu 41566, Republic of Korea.

Toxicological sciences : an official journal of the Society of Toxicology

|June 1, 2023

概括

暴露会导致丸损伤和不孕症,因为它会诱导细胞内网膜应激和精子细胞的亡. 向ATF6通路和p38 MAPK可能为引起的男性不孕症提供治疗策略.

科学领域:

生殖生物学生殖生物学
毒理学毒理学毒理学
细胞应激反应的应激反应

背景情况:

是一种有毒的重金属,已知会损害男性生殖功能.
细胞内膜网膜 (ER) 应激和亡与诱导的丸损伤有关.
展开的蛋白质反应 (UPR) 途径,包括ATF6,ATF4和XBP1s,参与细胞应激适应.

研究的目的:

为了阐明诱导的ER压力和精子细胞中亡的机制.
调查ATF6,ATF4和XBP1s通路在毒性中的作用.
探索ER压力和MAPK信号在诱导的男性不孕症之间的相互作用.

主要方法:

在精子细胞中过度表达p50ATF6,ATF4和拼接XBP1s以研究UPR.
通过siRNA介导的蛋白质表达的抑制,以评估亡减少.
在小鼠体内实验以验证在整个生物体中的发现.
对p38 MAPK酸化及其通过p50ATF6.6调节的分析.

主要成果:

激活转录因子6 (ATF6) 途径是ER应激和诱导的亡的主要媒介.
通过siRNA抑制蛋白质表达,在应激下显著降低了细胞亡.
在小鼠丸中对p50ATF6的升级加剧了诱导的亡.
p50ATF6强烈调节了p38 MAPK酸化,而p-p38调节了p50ATF6活动.

结论:

暴露于会诱导精子细胞亡,主要通过ATF6通路.
调节p38 MAPK和p50ATF6活性为诱导的男性不孕症提供了潜在的治疗方法.
了解ER压力-MAPK轴对于开发生殖毒性治疗方法至关重要.

关键词:

在ATF6中使用ATF6.灭症 (apoptosis) 是一种死亡的过程.和是的组成部分.细胞内膜网膜 (ER) 的压力压力.精子细胞精子细胞.

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