Related Experiment Video
Updated: Jul 23, 2026
Automated Measurement of Pulmonary Emphysema and Small Airway Remodeling in Cigarette Smoke-exposed Mice
Published on: January 16, 2015
Mechanistic Insights Into the Role of Selenoprotein M in Nickel-Induced Lung Fibrosis
Haoyue Guan1,2, Yue Sun1, Senqiu Qiao1
1College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, P. R. China.
Abstract:
Long-term exposure to high concentrations of nickel (Ni) compounds could cause damage to lung tissue and increase the risk of lung and respiratory cancers. Selenoprotein M (SELENOM) plays a crucial role in antioxidant and anti-inflammatory activities. However, the relationship between SELENOM and the mechanism of Ni-induced pulmonary fibrosis in mice remains unknown. Our study explored the regulated mechanism of SELENOM in Ni-induced pulmonary fibrosis. Wild-type and SELENOM knockout C57BL/6N male mice were randomly divided into Wild-control and Wild-Ni groups, which were administered distilled water and NiCl2 (10 mg/kg) by gavage for 21 days. Lung tissues were then collected for histological analysis using hematoxylin-eosin (H&E) and Masson staining, as well as for electron microscopic examination. Firstly, light microscopy revealed inflammatory cell infiltration, alveolar collapse, and alveolar wall thickening in the lung tissue of SELENOM knockout mice. Electron microscopy of lung tissue showed a large accumulation of fibroblasts, proliferation of collagen fibers, and dense collagen deposition, indicating that SELENOM knockout increased lung injury in Ni treatment. Secondly, SELENOM knockout increased malondialdehyde (MDA) levels while decreasing superoxide dismutase (SOD), total antioxidant capacity (T-AOC), and glutathione peroxidase (GSH-Px) activities. Furthermore, Ni exposure and SELENOM knockout significantly upregulated protein and mRNA levels of epithelial-mesenchymal transition (EMT) markers α-SMA, COL-I, TGF-β1/Smad, and JAK2/STAT3 signaling pathway in the lung. These findings suggest that SELENOM knockout promotes EMT and exacerbates pulmonary fibrosis and inflammation through activation of the TGF-β1/Smad and JAK2/STAT3 signaling pathways. In summary, our study highlights the critical role of SELENOM in mitigating Ni-induced pulmonary fibrosis and provides insights into potential therapeutic targets for Ni-induced lung diseases.
Insights
Selenoprotein M (SELENOM) deficiency worsens nickel-induced lung fibrosis by promoting inflammation and epithelial-mesenchymal transition (EMT) via TGF-β1/Smad and JAK2/STAT3 pathways.
Area of Science:
- Toxicology
- Cell Biology
- Pulmonary Medicine
Background:
- Nickel (Ni) compounds can cause lung damage and increase cancer risk.
- Selenoprotein M (SELENOM) possesses antioxidant and anti-inflammatory properties.
- The role of SELENOM in nickel-induced pulmonary fibrosis is not well understood.
Purpose of the Study:
- To investigate the mechanism of SELENOM in nickel-induced pulmonary fibrosis in mice.
- To determine how SELENOM deficiency affects lung injury and fibrosis progression.
Main Methods:
- Comparison of wild-type and SELENOM knockout mice exposed to nickel chloride (NiCl2).
- Histological analysis (H&E, Masson staining) and electron microscopy of lung tissues.
- Biochemical assays for oxidative stress markers (MDA, SOD, T-AOC, GSH-Px).
- Analysis of epithelial-mesenchymal transition (EMT) markers and signaling pathways (TGF-β1/Smad, JAK2/STAT3).
Main Results:
- SELENOM knockout exacerbated Ni-induced lung injury, characterized by inflammation, alveolar collapse, and fibrosis.
- Loss of SELENOM increased oxidative stress markers (MDA) and decreased antioxidant enzyme activities (SOD, T-AOC, GSH-Px).
- Ni exposure and SELENOM deficiency upregulated EMT markers (α-SMA, COL-I) and activated TGF-β1/Smad and JAK2/STAT3 signaling pathways.
Conclusions:
- SELENOM plays a protective role against nickel-induced pulmonary fibrosis.
- SELENOM deficiency promotes EMT and exacerbates lung inflammation and fibrosis through TGF-β1/Smad and JAK2/STAT3 activation.
- SELENOM may be a potential therapeutic target for nickel-induced lung diseases.
