Sirt1 m6A修改引起的莱迪格细胞衰老促进了Cd诱导的丸激素下降
Xin-Mei Zheng1, Xu-Dong Zhang2, Lu-Lu Tan2
1Department of Toxicology, School of Public Health, Center for Big Data and Population Health of IHM, Anhui Medical University, China; Key Laboratory of Environmental Toxicology of Anhui Higher Education Institutes, China; Key Laboratory of Population Health Across Life Cycle (Anhui Medical University), Ministry of Education of the People's Republic of China, China.
Ecotoxicology and environmental safety
|August 17, 2024
概括
暴露会通过诱导小鼠丸中的细胞衰老来降低. 这通过改变Sirtuin-1 (SIRT1) 表达和m6A修饰发生,影响男性生殖健康.
科学领域:
- 环境毒理学环境毒理学
- 内分泌学 在内分泌学.
- 细胞生物学 细胞生物学
背景情况:
- 降低丸激素与男性健康障碍有关.
- (Cd) 是一种环境重金属,可降低水平.
- 干扰丸激素合成的Cd的精确机制尚未完全理解.
研究的目的:
- 为了研究细胞衰老如何调解诱导的合成的抑制.
- 探索m6A修饰在这个过程中的作用.
- 为了确定诱导的低血的潜在治疗标.
主要方法:
- 暴露于C57BL/6N雄性小鼠和小鼠丸莱迪格细胞中的 (Cd).
- 评估水平,合成酶表达和细胞衰老标志物 (β-银酸酶,与衰老相关的蛋白质/表型).
- 对NAD依赖性脱乙酶Sirtuin-1 (SIRT1) 表达的分析,m6A修饰水平,以及METTL3和白醇的作用.
主要成果:
- 在小鼠中,CD暴露降低了水平和合成酶表达.
- Cd诱导了莱迪格细胞衰老,并降低了SIRT1的表达.
- Resveratrol治疗和SIRT1过度表达逆转了Cd的影响;Cd增加了METTL3和Sirt1的m6A修饰,而METTL3抑制恢复了SIRT1的表达.
结论:
- 暴露于会通过促进莱迪格细胞衰老来抑制小鼠丸中的合成.
- 这一过程是由SIRT1的m6A修饰介导的,受METTL3.3的影响.
- 准SIRT1和m6A修饰通路可能为环境毒素诱导的低丸血症提供治疗策略.
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