Cigarette smoke exposure is a major cause of chronic obstructive pulmonary disease (COPD), but the underlying molecular inflammatory mechanisms remain poorly understood. Previous studies have found that smoke disrupts cell-cell adhesion by inducing epithelial barrier damage to the adherens junction proteins, primarily E-cadherin (E-cad) and p120-catenin (p120). Recently, the antiinflammatory role of p120 has drawn increasing attention. In this study, we demonstrate that p120 has a role in the cigarette smoke extract-induced inflammatory response, presumably by regulating NF-kappa B signaling activation. Mechanistically, we show that p120-mediated NF-kappa B signaling activation in airway epithelial inflammation is partially RhoA dependent and is independent of E-cad. These results provide novel evidence for the role of p120 in the anti-inflammatory response.
基金：
National Natural Science Foundation of China [81070009]
第一作者单位：[1]Huazhong Univ Sci & Technol,Tongji Hosp,Tongji Med Coll,Inst Pathol,Wuhan 430030,Peoples R China
通讯作者：
推荐引用方式(GB/T 7714)：
Zhang Chao,Qin Shenghui,Qin Lingzhi,et al.Cigarette smoke extract-induced p120-mediated NF-κB activation in human epithelial cells is dependent on the RhoA/ROCK pathway[J].SCIENTIFIC REPORTS.2016,6:doi:10.1038/srep23131.
APA：
Zhang, Chao,Qin, Shenghui,Qin, Lingzhi,Liu, Liwei,Sun, Wenjia...&Wang, Xi.(2016).Cigarette smoke extract-induced p120-mediated NF-κB activation in human epithelial cells is dependent on the RhoA/ROCK pathway.SCIENTIFIC REPORTS,6,
MLA：
Zhang, Chao,et al."Cigarette smoke extract-induced p120-mediated NF-κB activation in human epithelial cells is dependent on the RhoA/ROCK pathway".SCIENTIFIC REPORTS 6.(2016)
