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Updated: May 26, 2025

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通过WTAP介导的m6Hmgb2的修改导致了PM2.5暴露引起的精子发生损伤

Jiankang Wang¹, Zhonghao Zhang², Fuquan Shi³

¹Institute of Toxicology, College of Preventive Medicine, State Key Lab of Trauma and Chemical Poisoning, Key Lab of Medical Protection for Electromagnetic Radiation, Ministry of Education of China, Army Medical University, Chongqing, 400038, China; Pancreatic Injury and Repair Key Laboratory of Sichuan Province, The General Hospital of Western Theater Command, Chengdu, 610083, China.

Environmental pollution (Barking, Essex : 1987)

|February 23, 2025

概括

细颗粒物 (PM2.5) 暴露会通过改变N6-甲基氨酸 (m6A) 表观遗传修饰,特别是减少WTAP甲基酶和影响Hmgb2基因表达来破坏精子的生产和运动,这对精子生成至关重要.

科学领域:

生殖生物学生殖生物学
环境表观遗传学环境表观遗传学
毒理学毒理学毒理学

背景情况:

N6-甲基氨酸 (m6A) 修改对于精子生成至关重要,对环境因素敏感.
众所周知,细颗粒物 (PM2.5) 伤害男性生殖系统,但潜在的表观遗传机制尚不清楚.

研究的目的:

研究m6A修饰在PM2.5引起的男性生殖功能障碍中的作用.
阐明特定的表观遗传机制,将PM2.5暴露与精子质量降低和精子生成功能障碍联系起来.

主要方法:

已建立的实时PM2.5暴露小鼠和GC-2spd细胞模型.
分析丸组织的m6A修饰变化,基因表达 (WTAP,Hmgb2) 和精子运动.
利用转录组测序来识别受影响的途径和基因功能.

主要成果:

暴露于PM2.5会导致精子产生的表皮损伤,线粒体异常和精子运动率降低.
不同的m6A修饰基因在精子生成途径中得到丰富;WTAP表达显著下降.
暴露于PM2.5减少了Hmgb2表达及其m6A修饰,影响精子细胞ATP水平;WTAP通过m6A调节Hmgb2mRNA稳定性.

结论:

暴露于PM2.5会破坏精子生成,并通过m6A修饰的表观遗传变化减少精子的运动性.
WTAP-m6A-Hmgb2轴是调解PM2.5诱导的男性生殖毒性的关键途径.
这些发现为空气污染对男性生育能力的表观遗传影响提供了新的见解.

关键词:

男人的生殖毒理学在PM{2.5) 中,精子运动性精子运动性 m(6) A6) 一个

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