Fine particulate matter exposure induces DNA damage by downregulating Rad51 expression in human bronchial epithelial Beas-2B cells in vitro
2020
Liu, Jiayu | Zhou, Jiaxin | Zhou, Jiazhen | Li, Mengcheng | Chen, Enzhao | Jiang, Guanqing | Chen, Yuyang | Wu, Jianjun | Yang, Qiaoyuan
Although an accumulating body of evidence suggests that fine particulate matter (PM₂.₅) can cause lung injury and lung cancer, the underlying mechanisms are not yet clear. In this study, multiple endpoints associated with the cellular response to PM₂.₅ exposure, including the cell proliferation rate, cell apoptosis, malondialdehyde (MDA) content and DNA damage, were evaluated in human bronchial epithelial Beas-2B cells. The mRNA expression profile in PM₂.₅-treated cells was analyzed by transcriptome sequencing. The DNA repair gene Rad51 was then selected for further analysis. We found that the viability and growth of Beas-2B cells decreased while cell apoptosis increased in a dose-dependent manner after PM₂.₅ exposure. The comet assay showed that PM₂.₅ exposure induced evident DNA damage in PM₂.₅-treated cells. The MDA content in the treated cells was increased, indicating that PM₂.₅ exposure promoted lipid peroxidation. Furthermore, Rad51 expression was downregulated in PM₂.₅-treated cells, which may have contributed to the PM₂.₅-induced DNA damage in Beas-2B cells. Upregulation of Rad51 expression could rescue the negative impact of PM₂.₅ exposure in Beas-2B cells. Taken together, our research demonstrates that PM₂.₅ exposure induces DNA damage and impairs the DNA repair process by downregulating Rad51 expression in Beas-2B cells. This finding is expected to provide new insight into the genotoxicity of PM₂.₅ exposure.
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