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Updated: Dec 29, 2025
A Silicosis Mouse Model Established by Repeated Inhalation of Crystalline Silica Dust
Published on: January 6, 2023
MiR-411-3p alleviates Silica-induced pulmonary fibrosis by regulating Smurf2/TGF-β signaling
Xuemin Gao1, Hong Xu2, Dingjie Xu2
1Basic Medical College, Hebei Medical Collage, Shijiazhuang, Hebei, 050017, China.
Abstract:
Occupational exposure to silica dust particles was the major cause of pulmonary fibrosis, and many miRNAs have been demonstrated to regulate target mRNAs in silicosis. In the present study, we found that a decreasing level of miR-411-3p in silicosis rats and lung fibroblasts induced by TGF-β1. Enlargement of miR-411-3p could inhibit the cell proliferation and migration in lung fibroblasts with TGF-β1 treatment and attenuate lung fibrosis in silicotic mice. In addition, a mechanistic study showed that miR-411-3p exert its inhibitory effect on Smad ubiquitination regulatory factor 2 (Smurf2) expression and decrease ubiquitination degradation of Smad7 regulated by smurf2, result in blocking of TGF-β/Smad signaling. We proposed that increased expression of miR-411-3p abrogates silicosis by blocking activation of TGF-β/Smad signaling through decreasing ubiquitination degradation effect of smurf2 on Smad7.
Insights
MicroRNA-411-3p (miR-411-3p) levels decrease in silicosis. Increasing miR-411-3p inhibits lung fibroblast proliferation and migration, potentially treating pulmonary fibrosis by blocking TGF-β/Smad signaling.
Area of Science:
- Biomedical Science
- Molecular Biology
- Occupational Health
Background:
- Silicosis, a severe lung fibrosis, stems from occupational silica dust exposure.
- MicroRNAs (miRNAs) play crucial roles in regulating gene expression in silicosis pathogenesis.
Purpose of the Study:
- To investigate the role of miR-411-3p in silicosis.
- To elucidate the underlying molecular mechanisms of miR-411-3p in regulating lung fibrosis.
Main Methods:
- Silicosis model in rats and TGF-β1-induced lung fibroblasts.
- Quantitative analysis of miR-411-3p expression.
- Assessment of cell proliferation and migration.
- Mechanistic studies involving Smad ubiquitination regulatory factor 2 (Smurf2) and Smad7.
Main Results:
- miR-411-3p levels were decreased in silicosis models.
- Upregulation of miR-411-3p inhibited fibroblast proliferation and migration.
- miR-411-3p suppressed Smurf2 expression, reducing Smad7 ubiquitination and degradation.
- This action effectively blocked the TGF-β/Smad signaling pathway.
Conclusions:
- miR-411-3p acts as a protective factor against silicosis.
- Restoring miR-411-3p levels may offer a therapeutic strategy for pulmonary fibrosis.
- The mechanism involves the inhibition of TGF-β/Smad signaling via Smurf2 and Smad7 regulation.
