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来自BEAS-2B细胞的外体中circRNAs放松调节与PM_2.5诱导的血管度有关

Qingping Liu¹, Yaling Zhang¹, Bin Han²

¹Department of Toxicology, Hebei Medical University, Shijiazhuang 050017, China.

Journal of environmental sciences (China)

|November 18, 2023

概括

细颗粒物 (PM2.5) 暴露会损害肺功能,并导致血管硬. 改变PM2.5的外体对内皮功能障碍有所贡献,揭示了心血管疾病的新机制.

科学领域:

环境健康环境健康
心血管研究研究心血管研究
分子生物学分子生物学

背景情况:

环境细颗粒物 (PM2.5) 与心血管疾病有关.
由于PM2.5引起的肺外疾病的分子机制尚不清楚.

研究的目的:

探索PM2.5对血管的不良影响,阐明潜在的分子机制.
研究外体在PM2.5引起的血管损伤中的作用.

主要方法:

建立了一个PM2.5暴露小鼠模型,并使用BEAS-2B细胞.
使用ceRNA数组和生物信息学分析了外体circRNA和mRNA.
构建了一个ceRNA网络并进行功能丰富分析.
实验验证了PM2.5衍生的外体体 (ExoPM2.5) 对内皮细胞的影响.

主要成果:

在小鼠中,暴露于PM2.5减少了肺功能,增加了血管硬.
在BEAS-2B细胞中的PM2.5诱导迁移和EMT.
在PM2.5-处理细胞释放的外体中鉴定出差异表达的circRNA和mRNA.
生物信息学分析显示,血管疾病相关途径的丰富.
特定的circRNAs (hsa_circ_0012627,hsa_circ_0053261,hsa_circ_0052810) 与内皮功能障碍有关.
ExoPM2.5实验诱导的内皮功能障碍,增加透性和减少放松.

结论:

暴露于PM2.5会导致血管硬和内皮功能障碍.
从暴露于PM2.5的细胞中衍生出来的外体细胞中介于内皮功能障碍.
这项研究阐明了PM2.5毒性和血管疾病病原性中的分子事件.

关键词:

内皮质功能障碍内皮质功能障碍异构体是什么? 异构体是什么? 外构体是什么?微细颗粒物质的细颗粒物质的细颗粒物质的细颗粒物质.血管硬化血管硬化这是一个 ceRNA 微阵列.

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