Academic Journal

Increased ERK signalling promotes inflammatory signalling in primary airway epithelial cells expressing Z {alpha}1-antitrypsin

التفاصيل البيبلوغرافية
العنوان: Increased ERK signalling promotes inflammatory signalling in primary airway epithelial cells expressing Z {alpha}1-antitrypsin
المؤلفون: van ‘t Wout, Emily F.A., Dickens, Jennifer A., van Schadewijk, Annemarie, Haq, Imran, Kwok, Hang Fai, Ordóñez, Adriana, Murphy, Gillian, Stolk, Jan, Lomas, David A., Hiemstra, Pieter S., Marciniak, Stefan J.
بيانات النشر: Oxford University Press
سنة النشر: 2014
المجموعة: HighWire Press (Stanford University)
مصطلحات موضوعية: ARTICLES
الوصف: Overexpression of Z α 1 -antitrypsin is known to induce polymer formation, prime the cells for endoplasmic reticulum stress and initiate nuclear factor kappa B (NF-κB) signalling. However, whether endogenous expression in primary bronchial epithelial cells has similar consequences remains unclear. Moreover, the mechanism of NF-κB activation has not yet been elucidated. Here, we report excessive NF-κB signalling in resting primary bronchial epithelial cells from ZZ patients compared with wild-type (MM) controls, and this appears to be mediated by mitogen-activated protein/extracellular signal-regulated kinase, EGF receptor and ADAM17 activity. Moreover, we show that rather than being a response to protein polymers, NF-κB signalling in airway-derived cells represents a loss of anti-inflammatory signalling by M α 1 -antitrypsin. Treatment of ZZ primary bronchial epithelial cells with purified plasma M α 1 -antitrypsin attenuates this inflammatory response, opening up new therapeutic options to modulate airway inflammation in the lung.
نوع الوثيقة: text
وصف الملف: text/html
اللغة: English
Relation: http://hmg.oxfordjournals.org/cgi/content/short/23/4/929; http://dx.doi.org/10.1093/hmg/ddt487
DOI: 10.1093/hmg/ddt487
الاتاحة: http://hmg.oxfordjournals.org/cgi/content/short/23/4/929
https://doi.org/10.1093/hmg/ddt487
Rights: Copyright (C) 2014, Oxford University Press
رقم الانضمام: edsbas.15AAD485
قاعدة البيانات: BASE