Abstract
Objective To investigate the influence of silica exposure on the expression of connective tissue growth factor (CTGF), transforming growth factor beta-1 (TGF-β1), and platelet-derived growth factor (PDGF) in lung silicosis rat. Methods Wistar rats were divided into an experimental group and a control group. In the experimental group, rats were exposed to silica by intratracheal instillation. In the control group, rats were exposed to physiological saline by intratracheal instillation. After 45 days, we compared the level of fibrosis and CTGF, TGF-β1, and PDGF in the lungs by immunohistochemistry or reverse transcription-polymerase chain reaction between the two groups. Results The results showed that the expression levels of CTGF, TGF-β1, and PDGF mRNA were significantly higher in the experimental group than those in the control group (P < 0.05). The positive staining of CTGF, TGF-β1, and PDGF mRNA was found in the cytoplasm, especially in the silicotic nodules of the hyalinisation section and cell endochylema of the alveolar macrophages, type II pneumonocytes, and lung tracheal epithelium. There were significantly positive correlations between CTGF, TGF-β1, and PDGF expressions (P < 0.05). A protein–protein interaction analysis showed interactions between TGF-β1, CTGF, and PDGF. Conclusions TGF-β/CTGF signaling pathway plays an important role in silicosis. Silicon dioxide exposure can induce the expression of CTGF, TGF-β1, and PDGF.
Highlights
Chronic silicosis is a common occupational disease caused by long-term inhaled silica dust at low levels in a dustproducing workplace
After 45 days of treatment, pathological foci of silicosis were observed in the lungs of all 20 rats instilled with dust in the experimental group; the lung volume of the silicosis group rats doubled, and the tissue texture was stiffer; oyster white needlepoint-like punctiform foci of infection were observed and felt stiffer when it was cut, and nodule felt like sand
The levels of connective tissue growth factor (CTGF), TGF-β1, and platelet-derived growth factor (PDGF) mRNA and proteins in the experimental group were all significantly higher than those in the controls (P < 0:05). These results suggest that silica exposure could stimulate the expression of these cytokines and that CTGF, TGF-β1, and PDGF might be involved in the pathogenesis of silicosis
Summary
Chronic silicosis is a common occupational disease caused by long-term inhaled silica dust at low levels in a dustproducing workplace. It is different from “accelerated silicosis,” in which the latency period is 5-10 years, and the “acute silicosis” which was caused by the exposure to high concentrations of silica for short periods [1]. The key point of this hypothesis is that inflammatory networks are activated when inhaled silica particles in the lungs are engulfed by macrophages, resulting in the release of inflammatory cytokines into the alveolar space [2].
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