The lncRNA H19/miR-29a-3p/SNIP1/c-myc regulatory axis is involved in pulmonary fibrosis induced by Nd2O3.
Autor: | Bu N; The Key Laboratory of Modern Toxicology of Ministry of Education, School of Public Health, Center for Global Health, Nanjing Medical University, Nanjing 211166, Jiangsu, PR China., Wang S; School of Public Health, Baotou Medical College, Baotou 014030, Inner Mongolia, PR China., Ma Y; School of Public Health, Baotou Medical College, Baotou 014030, Inner Mongolia, PR China., Xia H; The Key Laboratory of Modern Toxicology of Ministry of Education, School of Public Health, Center for Global Health, Nanjing Medical University, Nanjing 211166, Jiangsu, PR China., Zhao Y; School of Public Health, Baotou Medical College, Baotou 014030, Inner Mongolia, PR China., Shi X; School of Public Health, Baotou Medical College, Baotou 014030, Inner Mongolia, PR China., Liu Q; The Key Laboratory of Modern Toxicology of Ministry of Education, School of Public Health, Center for Global Health, Nanjing Medical University, Nanjing 211166, Jiangsu, PR China., Wang S; School of Public Health, Baotou Medical College, Baotou 014030, Inner Mongolia, PR China., Gao Y; School of Public Health, Baotou Medical College, Baotou 014030, Inner Mongolia, PR China. |
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Jazyk: | angličtina |
Zdroj: | Toxicological sciences : an official journal of the Society of Toxicology [Toxicol Sci] 2023 Dec 21; Vol. 197 (1), pp. 27-37. |
DOI: | 10.1093/toxsci/kfad107 |
Abstrakt: | Some rare earth elements are occupational and environmental toxicants and can cause organ and systemic damage; therefore, they have attracted global attention. Neodymium oxide (Nd2O3) is a rare earth element that is refined and significantly utilized in China. The long noncoding RNA (lncRNA) H19 is encoded by the H19/IGF2 imprinted gene cluster located on human chromosome 11p15.5. H19 has become a research focus due to its ectopic expression leading to the promotion of fibrosis. However, the mechanisms by which it causes pulmonary fibrosis are elusive. This investigation indicates that biologically active Nd2O3 increases H19, SNIP1, and c-myc, decreases miR-29a-3p, accelerates macrophage M2 polarization, and causes pulmonary fibrosis in mice lung tissues. In macrophage-differentiated THP-1 cells, Nd2O3 (25 μg/ml) enhanced H19, SNIP1, and c-myc, reduced miR-29a-3p, accelerated macrophages M2 polarization, and stimulated fibrogenic cytokine (TGF-β1) secretion. Furthermore, the coculturing of Nd2O3-treated macrophage-differentiated THP-1 cells. And human embryonic lung fibroblast cells activated lung fibroblast, which increases the levels of collagen I, α-SMA, p-Smad2/3, and Smad4, whereas H19 knockdown or miR-29a-3p upregulation in macrophages had opposite effects. Moreover, it was revealed that H19/miR-29a-3p/SNIP1/c-myc regulatory axis is involved in pulmonary fibrosis induced by Nd2O3. Therefore, this study provides new molecular insights into the mechanism of pulmonary fibrosis by Nd2O3. (© The Author(s) 2023. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.) |
Databáze: | MEDLINE |
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