Study on DNA methylation in HEB cells exposed to PM(2.5) by application of methylation chip technology.
10.3760/cma.j.cn121094-20201211-00684
- VernacularTitle:应用甲基化芯片技术研究PM
2.5对人支气管上皮细胞DNA甲基化水平影响
- Author:
Run Bing LI
1
;
Bing Yu WANG
1
;
Shuang Jian QIN
2
;
Xin Yun XU
3
;
Zhao Hui ZHANG
3
Author Information
1. School of Public Health, University of South China, Hengyang 421001, China Institute of Environment and Health, Shenzhen Center for Disease Control and Prevention, Shenzhen 518055, China.
2. Institute of Environment and Health, Shenzhen Center for Disease Control and Prevention, Shenzhen 518055, China Xiangya School of Public Health, Central South University, Changsha 410078, China.
3. School of Public Health, University of South China, Hengyang 421001, China.
- Publication Type:Journal Article
- Keywords:
Biomarkers;
DNA;
Fine particulate matter;
Genes;
Human bronchial epithelial cells;
Methylation
- MeSH:
Air Pollutants/toxicity*;
Basic Helix-Loop-Helix Transcription Factors/analysis*;
Carcinogenesis;
DNA Methylation;
Humans;
Particulate Matter/toxicity*;
Technology
- From:
Chinese Journal of Industrial Hygiene and Occupational Diseases
2022;40(3):177-182
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To screen the differential methylation sites, genes and pathways of air pollution fine particles (PM(2.5)) on human bronchial epithelial (HBE) cells by methylation chip and bioinformation technology, so as to provide scientific basis for further study of the toxicological mechanism of PM(2.5) on HBE cells. Methods: In August 2020, HBE cells were infected with 10 μg/ml and 50 μg/ml PM(2.5) aqueous solution for 24 h, namely PM(2.5) 10 μg/ml exposure group (low dose group) and PM(2.5) 50 μg/ml exposure group (high dose group) ; uninfected HBE cells were used as control group. The DNA fragments were hybridized with the chip, the chip scanned and read the data, analyzed the data, screened the differential methylation sites, carried out GO analysis and KEGG analysis of the differential methylation sites, and analyzed the interaction relationship of the overall differential methylation sites by functional epigenetic modules (FEMs). Results: Compared with the control group, 127 differential methylation sites were screened in the low-dose group, including 89 genes, including 55 sites with increased methylation level and 72 sites with decreased methylation level. The differential methylation sites were mainly concentrated in the Body region and UTR region. Compared with the control group, 238 differential methylation sites were screened in the high-dose group, including 168 genes, of which 127 sites had increased methylation level and 111 sites had decreased methylation level. The differential heterotopic sites were mainly concentrated in the Body region and UTR region. Through FEMs analysis, 8 genes with the most interaction were screened, of which 6 genes had significant changes in methylation level. MALT1 gene related to apoptosis was found in the heterotopic site of methylation difference in low-dose group; PIK3CA and ARID1A genes related to carcinogenesis were found in the heterotopic sites of methylation difference in high-dose group; TNF genes related to tumor inhibition were found in the results of FEMs analysis. Conclusion: After PM(2.5) exposure to HBE cells, the DNA methylation level is significantly changed, and genes related to apoptosis and carcinogenesis are screened out, suggesting that the carcinogenic mutagenic effect of PM(2.5) may be related to DNA methylation.
