Particulate matter (PM)(2.5) affects keratinocytes via endoplasmic reticulum (ER) stress-mediated suppression of apoptosis
- Authors
- Kim, J. H.; Son, J. W.; Kim, J.; Kim, M. G.; Jeong, S. H.; Park, T. J.; Son, S. W.; Ryu, H. J.
- Issue Date
- 4월-2020
- Publisher
- KOREAN SOCIETY TOXICOGENOMICS & TOXICOPROTEOMICS-KSTT
- Keywords
- Particulate matter (PM); Psoriasis; Cell proliferation; Endoplasmic reticulum (ER) stress; Apoptosis
- Citation
- MOLECULAR & CELLULAR TOXICOLOGY, v.16, no.2, pp.129 - 137
- Indexed
- SCIE
SCOPUS
KCI
- Journal Title
- MOLECULAR & CELLULAR TOXICOLOGY
- Volume
- 16
- Number
- 2
- Start Page
- 129
- End Page
- 137
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/56697
- DOI
- 10.1007/s13273-019-00065-6
- ISSN
- 1738-642X
- Abstract
- 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.
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