著作: Liu Yingqi/Wei Haiyan/Tang Jing/Yuan Jiaming/Wu Mingmin/[姚 陳娟]/[細井 和雄]/Yu Shali/Zhao Xinyuan/Han Yu/Chen Gang/Dysfunction of pulmonary epithelial tight junction induced by silicon dioxide nanoparticles via the ROS/ERK pathway and protein degradation./[Chemosphere]
(英) Dysfunction of pulmonary epithelial tight junction induced by silicon dioxide nanoparticles via the ROS/ERK pathway and protein degradation.
(英) Silica nanoparticles (SiNPs) are one of the most widely used types of nanoparticles across many industrial sectors, and are known to be present in the air year-round. In this study, we aimed to evaluate the potential adverse effects of SiNP exposure on pulmonary epithelial tight junctions, which serve as a critical barrier between the respiratory system and the circulatory system. In vivo studies confirmed that SiNPs decreased the protein expression levels of zonula occludens 1 (ZO-1), zonula occludens 2 (ZO-2), and occludin in the lungs of C57BL/6 mice. In vitro studies showed that SiNPs not only decreased the mRNA and protein expression of ZO-1 and ZO-2, but also decreased the protein expression of occludin in human bronchial epithelial (BEAS-2B) cells. In addition, SiNP exposure increased reactive oxygen species (ROS) production and activated extracellular regulated protein kinases (ERKs) and c-Jun N-terminal kinase (JNK). The inhibition of ROS and ERKs effectively protected the SiNP-induced downregulation of ZO-1 mRNA and protein expression, but had no effect on ZO-2 or occludin expression. SiNP-induced matrix metalloproteinase 9 (MMP9) protein expression appeared to be involved in occludin proteolytic degradation, in addition to SiNP-induced direct occludin protein degradation. The present study suggests that SiNPs disturb pulmonary epithelial tight junction structure and function via the ROS/ERK pathway and protein degradation.
|年月日||必須||2020年 5月 3日|