Dataset Information

Cigarette smoke extract-induced p120-mediated NF-?B activation in human epithelial cells is dependent on the RhoA/ROCK pathway.

ABSTRACT: 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 anti-inflammatory 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-?B signaling activation. Mechanistically, we show that p120-mediated NF-?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.

SUBMITTER: Zhang C

PROVIDER: S-EPMC5009380 | biostudies-literature | 2016 Sep

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Cigarette smoke extract-induced p120-mediated NF-κB activation in human epithelial cells is dependent on the RhoA/ROCK pathway.

Zhang Chao C Qin Shenghui S Qin Lingzhi L Liu Liwei L Sun Wenjia W Li Xiyu X Li Naping N Wu Renliang R Wang Xi X

Scientific reports 20160902

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 anti-inflammatory role of p120 has drawn increasing attention. In this study, we demonstrate that p120 has a role in the c ...[more]

PMID: 27586697

Similar Datasets

Project description:Chronic obstructive pulmonary disease (COPD) is a prevalent and long-term airway disease. It has been reported that fucoxanthin (FX) exhibits anti-inflammatory and antioxidant effects. However, the underlying mechanism of FX in COPD remains unknown. Therefore, to investigate the effect of FX on COPD, BEAS-2B cells were treated with cigarette smoke extract (CSE). The viability of BEAS-2B cells treated with increasing doses of FX was assessed by Cell Counting Kit-8. Lactate dehydrogenase (LDH) levels were measured using a corresponding kit. In addition, ELISA was carried out to detect the content of TNF-α, IL-1β and IL-6. Additionally, a TUNEL assay and western blot analysis were performed to assess the cell apoptosis rate. Furthermore, 2',7'-dichlorodihydrofluorescein diacetate was used to measure reactive oxygen species levels, while the contents of oxidative stress-associated indexes were determined using the corresponding kits. Bioinformatics analysis using the search tool for interactions of chemicals database predicted that peroxisome proliferator-activated receptor γ (PPARγ) may be a target of FX. The binding capacity of FTX with PPARγ was confirmed by molecular docking. The protein expression levels of the PPARγ/NF-κB signaling-associated factors were detected by western blot analysis. Finally, the regulatory mechanism of FX in COPD was revealed following cell treatment with the PPARγ inhibitor, T0070907. The results demonstrated that FX enhanced CSE-induced BEAS-2B cell viability and attenuated CSE-induced BEAS-2B cell inflammation and oxidative damage, possibly via triggering PPARγ/NF-κB signaling. Pre-treatment of BEAS-2B cells with the PPARγ inhibitor, T0070907, could reverse the protective effects of FX on CSE-induced BEAS-2B cells. Overall, the present study suggested that FX could ameliorate oxidative damage as well as inflammation in CSE-treated human bronchial epithelial in patients with COPD via modulating the PPARγ/NF-κB signaling pathway.

Dataset Information

Cigarette smoke extract-induced p120-mediated NF-?B activation in human epithelial cells is dependent on the RhoA/ROCK pathway.

Publications

Cigarette smoke extract-induced p120-mediated NF-κB activation in human epithelial cells is dependent on the RhoA/ROCK pathway.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets