Jeong, Seung-Chan Shin, Chan-Young Song, Mi-Kyung Cho, Yoon Ryu, Jae-Chun 2024-01-20T08:03:29Z 2024-01-20T08:03:29Z 2021-09-05 2014-12-31 1738-642X https://pubs.kist.re.kr/handle/201004/125974 Many epidemiological and in vitro studies have shown that particulate matter 2.5 (PM2.5) is associated with adverse health effects in humans, especially respiratory morbidity and mortality(1-3). While the mechanisms for these effects have been vigorously investigated for many years, they still remain uncertain. In previous studies, we collected PM2.5 samples in Seoul, Korea, where pollution results from a high level of automobile traffic, and analyzed the chemical composition of PM2.5. In the present study, we used gene expression profiling and gene ontology (GO) analysis to identify the gene expression changes in A549 human alveolar epithelial cells induced by exposure to water and organic extracts of PM2.5 (W-PM2.5 and O-PM2.5) in order to evaluate the adverse health effects of PM2.5. Transcriptomic profiling indicates that the O-PM2.5 exposure group was more sensitive in gene alterations than the W-PM2.5 exposure group. Through analysis of gene expression profiles, we identified 149 W-PM2.5-specific genes and 516 O-PM2.5-specific genes, as well as 173 commonly expressed genes in both the W-PM2.5 and O-PM2.5 exposure groups. After gene ontology (GO) analysis on the O-PM23-specific genes, we determined several key pathways that are known to be related to increasing pulmonary toxicity, such as immune response, regulation of inflammatory response, metabolism of xenobiotics by cytochrome P450, and retinol metabolism. However, we did not find the pulmonary toxicity-related pathways through GO analysis on the W-PM2.5-specific genes. In addition, 173 commonly expressed genes are involved in tyrosine catabolic process, retinol metabolism pathway, and steroid hormone biosynthesis - all of which are known to induce adverse health effects. In conclusion, this report describes changes in gene expression profiles in an in vitro respiratory system in response to exposure to PM2.5 water and organic extracts and relates these gene expression changes to pulmonary toxicity related pathways. This experiment adds to the understanding of how cells respond to PM2.5 exposure through transcriptional regulation. English KOREAN SOCIETY TOXICOGENOMICS & TOXICOPROTEOMICS-KSTT BLADDER-CANCER POLYMORPHISMS CYP1A1 ASSOCIATION METABOLISM INDUCTION ACID Gene expression profiling of human alveolar epithelial cells (A549 cells) exposed to atmospheric particulate matter 2.5 (PM2.5) collected from Seoul, Korea Article 10.1007/s13273-014-0040-9 1 MOLECULAR & CELLULAR TOXICOLOGY, v.10, no.4, pp.361 - 368 MOLECULAR & CELLULAR TOXICOLOGY 10 4 361 368 scie scopus kci 000347497100003 2-s2.0-84921369629 Biochemistry & Molecular Biology Toxicology Biochemistry & Molecular Biology Toxicology Article BLADDER-CANCER POLYMORPHISMS CYP1A1 ASSOCIATION METABOLISM INDUCTION ACID Particulate matter 2.5 (PM2.5) Microarray Gene ontology (GO) Pulmonary toxicity