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在柴油机排气颗粒引起的甲状腺细胞之间的粘合功能障碍中,整合素α3β1的作用背后的机制
Xiaoyin Guo1, Siying Tang2, Yanting Li1
1School of Public Health, Qingdao University, Qingdao, China.
The Science of the total environment
|July 7, 2024
概括
柴油废气颗粒 (DEP) 暴露会损害小鼠甲状腺结构和功能. 这种损伤涉及受损的细胞粘附通路,特别是CD151/整蛋白α3β1/Rac1通路,导致甲状腺损伤.
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:
- 柴油废气颗粒 (DEP) 是常见的环境污染物.
- 通过DEP诱导甲状腺损伤的具体机制尚不清楚.
研究的目的:
- 在小鼠模型中研究DEP暴露对甲状腺结构和功能的影响.
- 阐明DEP诱导的甲状腺损伤的潜在分子机制,重点关注细胞粘附途径.
主要方法:
- 在体内暴露于DEP的小鼠模型.
- 甲状腺组织的组织病理学检查.
- 甲状腺激素合成蛋白质表达的分析 (甲状腺过氧化酶,甲状腺球蛋白).
- 测量血清甲状腺激素水平 (triiodothyronine,tetraiodothyronine) 和TSH的水平.
- 基格路径丰富分析.
- 免疫光和体外细胞粘附测试.
主要成果:
- 暴露于DEP造成了显著的甲状腺毛囊结构损伤,包括破裂和体溢出.
- 甲状腺过氧化酶和甲状腺球蛋白的表达减少与结构损伤相关.
- 观察到血清三甲氨酸和四甲氨酸水平升高.
- 凯格分析和实验数据表明细胞粘附的变化,涉及整合素α3β1,CD151和Rac1.
- 暴露于DEP会损害甲状腺细胞粘附,通过CD151/α3β1/Rac1通路进行介导.
结论:
- 暴露于DEP会引起甲状腺结构和功能损伤.
- CD151/整蛋白α3β1/Rac1通路在DEP诱导的甲状腺细胞粘附破坏和随后的腺体损伤中发挥着关键作用.
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