Xu Rui, Li Qi, Zhou Xiang-Dong, Perelman Juliy M, Kolosov Victor P
Department of Respiratory Medicine, the Second Affiliated Hospital, Chongqing University of Medical Science, Chongqing 400010, China.
Int J Mol Sci. 2013 Apr 29;14(5):9475-86. doi: 10.3390/ijms14059475.
Oxidative stress has been implicated as an important contributing factor in the pathogenesis of several pulmonary inflammatory diseases. Previous studies have indicated a relationship between oxidative stress and the attenuation of epithelial tight junctions (TJs). In Human Bronchial Epithelial-16 cells (16HBE), we demonstrated the degradation of zonula occludens-1 (ZO-1), and claudin-2 exhibited a great dependence on the activation of the transient receptor potential melastatin (TRPM) 2 channel, phospholipase Cγ1 (PLCγ1) and the protein kinase Cα (PKCα) signaling cascade.
氧化应激被认为是几种肺部炎症性疾病发病机制中的一个重要促成因素。先前的研究表明氧化应激与上皮紧密连接（TJ）的减弱之间存在关联。在人支气管上皮-16细胞（16HBE）中，我们证明了闭合蛋白-1（ZO-1）的降解，并且紧密连接蛋白-2对瞬时受体电位香草酸亚型1（TRPM）2通道、磷脂酶Cγ1（PLCγ1）和蛋白激酶Cα（PKCα）信号级联的激活表现出极大的依赖性。
