ATF3调解PM2.5诱导的亡和卵巢颗粒细胞的炎症
Xiandan Zhang1, Xuan Wang2, Hao Li3
1Department of Gynecology and Obstetrics, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China.
Journal of ovarian research
|November 5, 2024
概括
颗粒物2.5 (PM2.5) 暴露会通过引起炎症和细胞死亡来损害卵巢功能. 激活转录因子3 (ATF3) 途径被确定为PM2.5诱导的卵巢损伤中的关键机制.
科学领域:
- 环境健康 环境健康
- 生殖毒理学 生殖毒理学
- 分子生物学分子生物学
背景情况:
- 颗粒物2.5 (PM2.5) 是一个重要的全球健康风险.
- 以前的研究表明,PM2.5会损害卵巢功能,但机制尚不清楚.
- 了解PM2.5对卵巢健康的影响对于公众健康至关重要.
研究的目的:
- 调查PM2.5暴露导致卵巢损伤的机制.
- 为了确定涉及PM2.5诱导的卵巢损伤的特定基因和途径.
- 阐明激活转录因子3 (ATF3) 在PM2.5毒性的作用.
主要方法:
- 小鼠通过气管滴水暴露在PM2.5中,持续了5个月.
- 人类颗粒细胞 (KGN) 在体外用PM2.5进行了治疗.
- 进行RNA测序以确定分子变化.
- 机械学研究探讨了炎症,亡和ATF3.3之间的关联.
主要成果:
- 暴露于PM2.5导致小鼠的卵巢损伤,包括炎症和卵泡缩.
- PM2.5抑制了KGN细胞活力和诱导了细胞亡.
- RNA测序揭示了激活转录因子3 (ATF3) 表达的增加.
- 在PM2.5,亡,炎症,ATF3和氧化应激之间建立了联系.
结论:
- 在PM2.5引起的卵巢损伤中,ATF3通路具有关键作用.
- 暴露于PM2.5会通过ATF3通路触发卵巢细胞中的炎症和亡.
- 这些发现提供了与空气污染相关的生殖健康风险的见解.
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