上皮-间质转换
免疫印迹
下调和上调
波形蛋白
自噬
炎症
信号转导
细胞生物学
化学
污渍
NF-κB
癌症研究
免疫组织化学
免疫学
生物
细胞凋亡
生物化学
基因
作者
Yanpeng Ma,Qi‐Lian Liang,Fenghong Wang,Kanglin Yan,Mengqi Sun,Lisen Lin,Tianyu Li,Junchao Duan,Zhiwei Sun
标识
DOI:10.1016/j.ecoenv.2022.113303
摘要
It has been reported that silica nanoparticles (SiNPs) could cause epithelial-to-mesenchymal transition (EMT), but the specific mechanism is still unclear. Thus, the purpose of this study was to investigate the underlying mechanisms of pulmonary EMT after subacute exposure to SiNPs. The results showed intratracheal instillation of SiNPs increased the pulmonary MDA content, while decreased the activity of SOD and GSH-Px in rats. Western blot analysis demonstrated that SiNPs induced autophagy dysfunction via the upregulation of p62. Meanwhile, the inflammation cytokines (TNF-α, IL-18, IL-1β) were released in rat lung. Immunohistochemistry and western blot assays both showed that SiNPs could regulate the related protein biomarkers of EMT through decreasing E-cadherin and increasing vimentin in a dose-dependent manner. Besides, SiNPs activated the proteins expression involved in p62/NF-κB signaling pathway, whereas the pulmonary EMT induced by SiNPs was significantly dampened after the knock down of p62. In this study, we illustrated that subacute exposure to SiNPs could trigger the autophagy dysfunction and pulmonary inflammation, further lead to EMT via activating the p62/NF-κB signaling pathway. Our findings provide new molecular evidence for SiNPs-induced pulmonary toxicity.
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