SMAD公司
上皮-间质转换
转化生长因子
肺纤维化
Smad2蛋白
纤维化
癌症研究
化学
MAPK/ERK通路
信号转导
细胞生物学
医学
波形蛋白
下调和上调
内科学
生物
免疫组织化学
生物化学
基因
作者
Hongrui Guo,Zhijie Jian,Huan Liu,Hengmin Cui,Huidan Deng,Jing Fang,Zhicai Zuo,Xun Wang,Ling Zhao,Yi Geng,Ping Ouyang,Huaqiao Tang
标识
DOI:10.1016/j.taap.2021.115500
摘要
Copper (Cu) is considered as an essential trace element for living organisms. However, over-exposure to Cu can lead to adverse health effects on human and animals. There are limited researches on pulmonary toxicity induced by Cu. Here, we found that copper sulfate (CuSO4)-treatment could induce pulmonary fibrosis with Masson staining and up-regulated protein and mRNA expression of Collagen I and α-Smooth Muscle Actin (α-SMA) in mice. Next, the mechanism underlying Cu-induced pulmonary fibrosis was explored, including transforming growth factor-β1 (TGF-β1)-mediated Smad pathway, mitogen-activated protein kinases (MAPKs) pathway and epithelial-mesenchymal transition (EMT). CuSO4 triggered pulmonary fibrosis by activation of the TGF-β1/Smad pathway, which was accomplished by increasing TGF-β1, p-Smad2 and p-Smad3 protein and mRNA expression levels. Also, up-regulated protein and mRNA expression of p-JNK, p-ERK, and p-p38 demonstrated that CuSO4 activated MAPKs pathways. Concurrently, EMT was activated by increasing vimentin and N-cadherin while decreasing E-cadherin protein and mRNA expression levels. Altogether, the abovementioned findings indicate that CuSO4 treatment may induce pulmonary fibrosis through the activation of EMT induced by TGF-β1/Smad pathway and MAPKs pathways, revealing the mechanism Cu-caused pulmonary toxicity.
科研通智能强力驱动
Strongly Powered by AbleSci AI