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Establishing a Silicosis Rat Model via Exposure of Whole-Body to Respirable Silica
Published on: October 28, 2022
[Regulatory effect of miR-149 on interleukin-6 expression in silica-induced pulmonary fibrosis]
Jingjing Fan1, Xiaoming Ji1, Shasha Wang1
1Department of Occupational Medicine and Environmental Health, School of Public Health, Nanjing Medical University, Nanjing 210029, China.
Objective:
To investigate the regulatory effect of miR-149 on interleukin-6 (IL-6) expression in silica-induced pulmonary fibrosis.
Methods:
A mouse model of pulmonary fibrosis was established using silica dust; the level of miR-149 in the lung tissues of mice with silica-induced pulmonary fibrosis was measured by quantitative real-time polymerase chain reaction (qRT-PCR), while the protein expression of IL-6 was measured by immunohistochemistry and Western blot. Type II alveolar epithelial cells (A549) and bronchial epithelial cells (HBE) were exposed to silica dust to establish a model; the level of miR-149 was measured by qRT-PCR, while the protein expression of IL-6 was measured by Western blot. A549 cells were transfected with miR-149 mimics and inhibitor in vitro, and the cellular expression of IL-6 was measured by Western blot. Serum samples from patients with coal workers' pneumoconiosis were examined by double-antibody sandwich ELISA to measure the protein expression of IL-6.
Results:
At three time points after silica treatment, the miR-149 expression in lung tissues was significantly down-regulated while an evident increase in IL-6 expression was observed in lung tissues (P < 0.01). Silica-stimulated epithelial cell (A549 and HBE) had up-regulated IL-6 expression and down-regulated miR-149 expression (P < 0.01). Increased levels of miR-149 attenuated IL-6 expression, whereas adverse results were found when miR-149 was inhibited. Compared with that in control group, serum level of IL-6 was significantly increased in patients with stage II and III coal workers' pneumoconiosis (P < 0.01).
Conclusion:
Down-regulation of miR-149 and up-regulation of IL-6 might be involved in the progression of silica-induced pulmonary fibrosis; miR-149 could negatively regulate IL-6 expression.
Insights
MicroRNA-149 (miR-149) levels decrease while interleukin-6 (IL-6) increases in silica-induced pulmonary fibrosis. miR-149 negatively regulates IL-6, suggesting a role in disease progression.
Area of Science:
- Biomedical research
- Molecular biology
- Pulmonary medicine
Context:
- Silica exposure is a known cause of occupational lung disease.
- Pulmonary fibrosis is a debilitating condition characterized by lung scarring.
- Interleukin-6 (IL-6) is a pro-inflammatory cytokine implicated in fibrotic processes.
Purpose:
- To investigate the regulatory role of microRNA-149 (miR-149) in controlling interleukin-6 (IL-6) expression.
- To examine the relationship between miR-149 and IL-6 in the context of silica-induced pulmonary fibrosis.
- To assess miR-149 and IL-6 levels in both animal models and human patients with pneumoconiosis.
Summary:
- Silica exposure in mice led to decreased miR-149 and increased IL-6 in lung tissues and epithelial cells.
- In vitro experiments showed that miR-149 mimics reduced IL-6 expression, while miR-149 inhibitors increased it.
- Elevated serum IL-6 levels were observed in patients with coal workers' pneumoconiosis.
Impact:
- The findings suggest that the down-regulation of miR-149 and subsequent up-regulation of IL-6 are involved in the pathogenesis of silica-induced pulmonary fibrosis.
- miR-149 acts as a negative regulator of IL-6 expression, identifying it as a potential therapeutic target.
- This research contributes to understanding the molecular mechanisms underlying occupational lung diseases.
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