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Nicotine reduces the levels of surfactant proteins A and D via Wnt/β-catenin and PKC signaling in human airway epithelial cells
Publication date: 15 January 2016 Source:Respiratory Physiology & Neurobiology, Volume 221 Author(s): Weifeng Zou, Sha Liu, Jinxing Hu, Qing Sheng, Fang He, Bing Li, Pixin Ran A deficiency of surfactant proteins A and D has been proposed as a mechanism in airway remodeling, which is one characteristic of chronic obstructive pulmonary disease (COPD). We recently showed that in vitro nicotine exposure induces Wnt3a/β-catenin activation, which is a pathway that has also been implicated in altering levels of SP-A and SP-D. Nicotine induced activation of protein kinase C(PKC), and the involvement of PKC in med...
Source: Respiratory Physiology and Neurobiology - October 30, 2015 Category: Respiratory Medicine Source Type: research

Nicotine-induced epithelial-mesenchymal transition via Wnt/{beta}-catenin signaling in human airway epithelial cells
Epithelial-mesenchymal transition (EMT) has been proposed to be a mechanism in airway remodeling, which is a characteristic of chronic obstructive pulmonary disease (COPD). Studies have shown that cigarette smoke and nicotine are factors that induce Wnt/β-catenin activation, which is a pathway that has also been implicated in EMT. The main aim of this study was to test whether human bronchial epithelial cells are able to undergo EMT in vitro following nicotine stimulation via the Wnt3a/β-catenin signaling pathway. We show that nicotine activates the Wnt3a signal pathway, which leads to the translocation of β...
Source: AJP: Lung Cellular and Molecular Physiology - February 15, 2013 Category: Respiratory Medicine Authors: Zou, W., Zou, Y., Zhao, Z., Li, B., Ran, P. Tags: CALL FOR PAPERS Source Type: research