Metabolic changes during epithelial-mesenchymal transition in the lungs of silicosis mice
10.20001/j.issn.2095-2619.20260201
- VernacularTitle:矽肺模型小鼠肺部上皮-间质转化过程中的代谢变化
- Author:
Huifan YANG
1
;
Jianling SHEN
;
Ping WANG
;
Yiru QIN
;
Qianyu WANG
;
Na ZHAO
Author Information
1. School of Public Health, Southern Medical University, Guangzhou, Guangdong 510515, China
- Publication Type:Journal Article
- Keywords:
Silica;
Silicosis;
Epithelial-mesenchymal transition;
Cadherin;
Vimentin;
Glycerophospholipid metabolism;
Metabolomics;
Mouse
- From:
China Occupational Medicine
2026;53(1):1-7
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the alterations in metabolic molecules and pathways during epithelial-mesenchymal transition (EMT) in the lungs of mice induced by silica exposure. Methods A total of 30 specific pathogen-free male C57BL/6 mice were randomly divided into a control group and a silicosis model group. Mice were intratracheally instilled with 40 µL of either 0.9% sodium chloride solution or silica suspension at a mass concentration of 125 g/L. At 7, 14, and 28 days post-exposure, five mice from each group were sacrificed to evaluate lung histopathological changes. The mRNA expression of EMT-related genes was measured by real-time quantitative polymerase chain reaction. Untargeted metabolomics was used to identify metabolites in mouse lung tissues, and differential metabolites (DMs) and metabolic pathways were analyzed. Results Following silica exposure, lung tissues of mice in the silicosis model group showed progressively aggravated pathological changes, including increased inflammatory cell infiltration, thickening of alveolar walls, collagen deposition, and progressive pulmonary fibrosis, with typical silicotic nodules forming by day 28. The Ashcroft scores and the mRNA expression of cadherin (Cdh)2 and vimentin of mice in the silicosis model group increased (all P<0.05), along with decreased Cdh1 mRNA expression compared with the control group at all the three time points (all P<0.05). The Ashcroft scores and the mRNA expression of Cdh2 and vimentin of mice in the silicosis model group increased with the increase of observation time after silica exposure (all P<0.05), while mRNA expression of Cdh1 decreased (all P<0.05). Metabolomics analysis indicated that silica exposure specifically altered the expression of lipids and disrupted multiple metabolic pathways during EMT in lung tissues of silicosis model group mice,with glycerophospholipid metabolism being most obviously affected (P<0.05). Conclusion Silica exposure may induce EMT in mouse lung tissue, resulting in pulmonary fibrosis in a time-dependent manner. The underlying mechanism may be associated with silica-induced disturbances in glycerophospholipid metabolism in mouse lung tissue.
