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暴露于PM2.5会诱导ARPE-19细胞的转录基因变化,并激活TGFβ介导的信号通路:下一代测序方法

Chueh-Tan Chen^1,2,3, Zhi-Hu Lin^2,3, Tung-Yi Lin^3,4

¹Department of Health and Welfare, University of Taipei, Taipei, Taiwan, ROC.

Journal of the Chinese Medical Association : JCMA

|September 12, 2025

概括

细颗粒物 (PM2.5) 暴露会改变视网膜色素表皮 (RPE) 细胞中的基因表达,激活转化生长因子-β (TGF-β) 途径并增加细胞迁移. 血管蛋白样4 (ANGPTL4) 被确定为这个过程中的关键调解者.

科学领域:

眼科医生眼科眼科
环境健康环境健康
分子生物学分子生物学

背景情况:

环境细颗粒物 (PM2.5) 对眼睛健康构成重大环境风险.
通过PM2.5影响视网膜色素上皮质 (RPE) 的分子机制尚不清楚.

研究的目的:

研究暴露于PM2.5.5的RPE细胞中的转录组变化.
确定PM2.5诱导的RPE变化所涉及的关键调节途径.

主要方法:

下一代测序 (NGS) 用于ARPE-19细胞的差异基因表达分析.
生物信息分析 (通路丰富,GSEA) 确定了受影响的信号通路.
进行了功能性测试 (活力,迁移) 和分子验证 (RT-PCR,ELISA).

主要成果:

暴露于PM2.5显著改变了基因表达,激活了细胞迁移途径 (焦点粘附,actin细胞骨架,ECM受体相互作用,紧结,粘附结).
调节了转化生长因子-β (TGF-β),MAPK和PI3K/AKT通路.
PM2.5增强了ARPE-19细胞活力和迁移; ANGPTL4被上调并依赖于TGF-β信号传递.

结论:

PM2.5诱导转录基因重编程,并激活RPE细胞中的TGF-β信号,增强迁移.
ANGPTL4是PM2.5暴露的RPE细胞中TGF-β的关键下游效应因子.
这项研究提供了关于空气污染在视网膜疾病中的作用和潜在的治疗点的见解.

关键词:

ANGPTL4 在线观看对于PM2.5来说,这是一个很好的例子.视网膜色素表皮细胞的细胞表皮.在TGF-β的基础上.

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TGF - β Signaling Pathway

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