Objective. In order to investigate the effects of PM2.5 on proliferation, cell cycle, apoptosis, and potential mechanism of human keratinocyte cell line HaCaT. Methods. HaCaT cells were treated with different concentrations of PM2.5 suspension for 24 hours. Cell viability was detected by the CCK-8 method. Cell cycle distribution and apoptosis were detected by flow cytometry. Microarray analyses were used to find out the microarray gene expression profiling; data processing included gene enrichment and pathway analysis. Western blot was conducted to validate the key pathways and regulators in the microarray analysis. Results. The cell activity decreased, and the cell cycle was significantly inhibited with the increase in PM2.5 concentration. Also, by conducting the gene expression microarray assay, we identified 541 upregulated genes and 935 downregulated genes in PM2.5-treated HaCaT cells. Real-time qPCR and western blot confirmed that PM2.5 treatment could induce the expression of ABCA1 while inhibiting that of END1 and CLDN1. Conclusion. Our results showed that PM2.5 could potentially regulate cell apoptosis and cell cycle arrest via ABCA1-, END1-, ID1-, and CLDN1-mediated pathways in human HaCaT cells, which laid a good foundation for follow-up drug intervention and drug development against skin damage caused by PM2.5 exposure.

中文翻译：

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PM2.5诱导的HaCaT细胞中ABCA1差异表达基因的鉴定及病理生理相关性的阐明

客观。为探讨PM2.5对人角质形成细胞系HaCaT增殖、细胞周期、凋亡的影响及潜在机制。方法。HaCaT 细胞用不同浓度的 PM2.5 悬浮液处理 24 小时。通过CCK-8方法检测细胞活力。流式细胞仪检测细胞周期分布和细胞凋亡。微阵列分析用于找出微阵列基因表达谱；数据处理包括基因富集和通路分析。进行蛋白质印迹以验证微阵列分析中的关键途径和调节剂。结果. 随着PM2.5浓度的升高，细胞活性降低，细胞周期明显受到抑制。此外，通过进行基因表达微阵列分析，我们在 PM2.5 处理的 HaCaT 细胞中鉴定了 541 个上调基因和 935 个下调基因。实时 qPCR 和蛋白质印迹证实 PM2.5 处理可以诱导 ABCA1 的表达，同时抑制 END1 和 CLDN1 的表达。结论。我们的研究结果表明，PM2.5可能通过ABCA1-、END1-、ID1-和CLDN1介导的途径在人HaCaT细胞中调节细胞凋亡和细胞周期阻滞，为后续药物干预和药物开发奠定了良好的基础。防止因 PM2.5 暴露造成的皮肤损伤。