Molecular & Cellular Toxicology ( IF 1.1 ) Pub Date : 2020-01-08 , DOI: 10.1007/s13273-019-00065-6 J. H. Kim , J. W. Son , J. Kim , M. G. Kim , S. H. Jeong , T. J. Park , S. W. Son , H. J. Ryu
Background
Particulate matter (PM)2.5 is a concern for public health nowadays. Although few studies have reported the skin diseases associated with PM2.5, its effects on keratinocytes have yet to be elucidated.
Objective
The goal of this experiment was to analyze and identify the changes of gene expression in PM2.5-treated keratinocytes using RNA-sequencing (RNA-Seq) data.
Results
PM2.5-treated keratinocytes exhibited changes in cell cycle-related genes as well as genes involved in DNA replication, endoplasmic reticulum (ER) stress, intrinsic apoptosis, and immune response. A total of 669 genes showed changes in gene expression in PM2.5-treated keratinocytes, including 304 upregulated and 365 downregulated genes.
Conclusion
Unlike other studies investigating skin disorders associated with PM2.5, our study found the mechanism of apoptosis suppression in keratinocytes. The findings may provide a novel insight into the management of chronic skin diseases in relation to PM2.5.
中文翻译:
颗粒物(PM)2.5通过内质网(ER)应激介导的凋亡抑制作用影响角质形成细胞
背景
颗粒物(PM)2.5是当今公共卫生的关注点。尽管很少有研究报道与PM 2.5有关的皮肤疾病,但其对角质形成细胞的作用尚未阐明。
目的
该实验的目的是使用RNA测序(RNA-Seq)数据分析和鉴定PM2.5处理的角质形成细胞中基因表达的变化。
结果
PM 2.5处理的角质形成细胞在细胞周期相关基因以及与DNA复制,内质网(ER)应激,内在凋亡和免疫反应有关的基因中均表现出变化。总共669个基因在PM 2.5处理的角质形成细胞中显示出基因表达的变化,包括304个上调的基因和365个下调的基因。
结论
与其他研究与PM 2.5相关的皮肤疾病的研究不同,我们的研究发现了角质形成细胞凋亡抑制的机制。这些发现可能为与PM 2.5相关的慢性皮肤病的治疗提供新颖的见解。