The widespread use of neodymium oxide nanoparticles (NPs-NdO) has caused environmental pollution and human health problems, thus attracting significant attention. Understanding the mechanisms of NPs- NdO-induced genetic damage is of great significance for identifying early markers for NPs- NdO-induced lung injury. At present, the mechanisms underlying DNA damage induced by NPs- NdO remain unclear. In this study, we performed functional assays on human bronchial epithelial cells (16HBEs) exposed to various concentrations of NPs-NdO and SD rats administered with a single intratracheal instillation with NPs-NdO. Exposure to NPs-NdO could lead to DNA damage in 16HBE cells and rat lung tissue cells. We found a novel long non-coding RNA, named CNTFR-AS1, which was highly expressed after exposure to NPs-NdO. Our data verified that transcription factor TP63 mediates the high expression levels of CNTFR-AS1, which in turn regulates NPs-NdO-induced DNA damage in cells by inhibiting HR repair. Moreover, the levels of CNTFR-AS1 were correlated with the number of years worked by occupational workers. Collectively, these results demonstrate that CNTFR-AS1 acts as a novel DNA damage regulator in bronchial epithelial cells exposed to NPs-NdO. Hence, our data provide a basis for the identification of lncRNAs as early diagnostic markers for rare earth lung injury.
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| http://dx.doi.org/10.1016/j.envpol.2023.122191 | DOI Listing |
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