Galectin 3 regulates silica-induced pulmonary fibrosis in mice via MAPK signalling pathway
- VernacularTitle:半乳糖凝集素-3通过MAPK信号通路调控二氧化硅诱导的小鼠肺纤维化
- Author:
Xinbei ZHOU
1
;
Xiaohan JIANG
2
;
Ningjuan LIANG
2
;
Xinru TU
2
Author Information
- Publication Type:Experiment
- Keywords: galectin-3; silicosis; MAPK signalling pathway; single-cell sequencing; pulmonary fibrosis
- From: Journal of Environmental and Occupational Medicine 2026;43(8):1027-1031
- CountryChina
- Language:Chinese
- Abstract: Background Silicosis is a progressive pulmonary fibrotic disease caused by long-term inhalation of silica (SiO2) dust, and abnormal fibroblast activation is a central pathological mechanism. Galectin 3 (LGALS3) plays a significant role in fibrosis across multiple organs; however, its specific molecular mechanism in SiO2-induced pulmonary fibrosis remains unclear. Objective To investigate the role of LGALS3 in silica (SiO2) induced pulmonary fibrosis and its potential molecular mechanisms. Methods Differentially expressed genes in mouse lung fibroblasts treated with SiO2 for 56 d were analysed using the GSE183682 single-cell RNA sequencing dataset, followed by pathway enrichment analysis. A mouse model of pulmonary fibrosis was established by intratracheal instillation of SiO2 suspension (50 mg·mL−1, 100 μL). Lung index, hydroxyproline content, and histopathological changes (HE staining) were assessed. Western blot and immunofluorescence staining were used to evaluate the expression of LGALS3, MAPK pathway proteins, and fibrosis markers [collagen type I alpha 1 chain (COL1A1) and α-smooth muscle actin (ACTA2)]. Results Single-cell RNA sequencing analysis identified 53 differentially expressed genes in fibroblasts, and Lgals3 was significantly upregulated in the SiO2 group. SiO2 exposure successfully induced pulmonary fibrosis in mice, as indicated by weight loss, elevated hydroxyproline content, alveolar structural disruption, and collagen deposition. Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses showed that Lgals3-associated genes were enriched in Toll-like receptor/chemokine signaling pathways. After SiO2 exposure, LGALS3 expression was increased in fibrotic lung tissue and co-localized with ACTA2, an activated fibroblast and myofibroblast marker. This was accompanied by activation of the MAPK signaling pathway. Conclusion LGALS3 may be involved in fibroblast activation and collagen deposition, potentially through activation of the MAPK signalling pathway. These findings suggest that LGALS3 may represent a potential regulatory target in SiO2-induced pulmonary fibrosis.
