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.
Original language | English |
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Pages (from-to) | 129-137 |
Number of pages | 9 |
Journal | Molecular and Cellular Toxicology |
Volume | 16 |
Issue number | 2 |
DOIs | |
Publication status | Published - 2020 Apr 1 |
Bibliographical note
Funding Information:This work was supported by the National Research Foundation of Korea Grant (NRF), funded by the Korean Government (NRF-2016R1C1B1014180) and Korea University Grants.
Funding Information:
This work was supported by the National Research Foundation of Korea Grant (NRF), funded by the Korean Government (NRF-2016R1C1B1014180) and Korea University Grants.
Publisher Copyright:
© 2019, The Korean Society of Toxicogenomics and Toxicoproteomics and Springer Nature B.V.
Keywords
- Apoptosis
- Cell proliferation
- Endoplasmic reticulum (ER) stress
- Particulate matter (PM)
- Psoriasis
ASJC Scopus subject areas
- Pathology and Forensic Medicine
- Toxicology
- Pharmacology, Toxicology and Pharmaceutics(all)
- Public Health, Environmental and Occupational Health
- Health, Toxicology and Mutagenesis