Kim, Woong Cho, Yoon Song, Mi-Kyung Lim, Jung-hee Kim, Jin Young Gye, Myung Chan Ryu, Jae-Chun 2024-01-19T21:31:59Z 2024-01-19T21:31:59Z 2021-09-05 2018-11 1520-4081 https://pubs.kist.re.kr/handle/201004/120740 Particulate matter the environmental toxicant, with a diameter less than or equal to 2.5 m (PM2.5) is a common cause of several respiratory diseases. In recent years, several studies have suggested that PM2.5 can influence diverse diseases, such as respiratory diseases, cardiovascular diseases, metabolic diseases, dementia, and female reproductive disorders, and unhealthy birth outcomes. In addition, several epidemiological studies have reported that adverse health effects of PM2.5 can differ depending on regional variations. In the present study, to evaluate specific adverse health effects of PM2.5, we collected two different PM2.5 samples from an underground parking lot and ambient air, and we evaluated cytotoxicity with eight different cell lines originating from human organs. Then, we selected JEG-3 human placenta cells, which show high cytotoxicity to both PM samples. Through RNA sequencing, gene expression profiling, and a gene ontology (GO) analysis of JEG-3 after exposure to two different PM2.5 samples, we identified 1021 commonly expressed genes involved in immune responses, the regulation of apoptosis, and so forth, which are known to induce several adverse health effects. In addition, we identified genes related to the calcium-signaling pathway, steroid hormone biosynthesis, and the cytokine-cytokine receptor interaction through a Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. Then, we confirmed these gene expressions using qRT-PCR, and the protein levels of mitogen-activated protein kinases and COX-2 with progesterone decreased using western blotting and enzyme-linked immunosorbent assay. In conclusion, this study suggests the possible toxic mechanism of human placenta that might be associated with PM2.5-induced female reproductive disorders. English WILEY NF-KAPPA-B AIR-POLLUTION COX-2 EXPRESSION P38 MAPK PROGESTERONE INHIBITION PM2.5 ACTIVATION MECHANISMS PATHWAYS Effect of particulate matter 2.5 on gene expression profile and cell signaling in JEG-3 human placenta cells Article 10.1002/tox.22591 1 ENVIRONMENTAL TOXICOLOGY, v.33, no.11, pp.1123 - 1134 ENVIRONMENTAL TOXICOLOGY 33 11 1123 1134 scie scopus 000447389900005 2-s2.0-85050724890 Environmental Sciences Toxicology Water Resources Environmental Sciences & Ecology Toxicology Water Resources Article NF-KAPPA-B AIR-POLLUTION COX-2 EXPRESSION P38 MAPK PROGESTERONE INHIBITION PM2.5 ACTIVATION MECHANISMS PATHWAYS cytokine female reproductive disorder mitogen-activated protein kinase particulate matter 2.5 steroid hormone synthesis