Abstract
Acetylcholine (ACh), synthesized by Choline Acetyl-Transferase (ChAT), exerts its physiological effects via mAChRM3 in epithelial cells. We hypothesized that cigarette smoke affects ChAT, ACh, and mAChRM3 expression in the airways from COPD patients promoting airway disease. ChAT, ACh, and mAChRM3 were assessed: "ex vivo" in the epithelium from central and distal airways of COPD patients, Healthy Smoker (S) and Healthy Subjects (C), and "in vitro" in bronchial epithelial cells stimulated with cigarette smoke extract (CSE). In central airways, mAChRM3, ChAT, and ACh immunoreactivity was significantly higher in the epithelium from S and COPD than in C subjects. mAChRM3, ChAT, and ACh score of immunoreactivity was high in the metaplastia area of COPD patients. mAChRM3/ChAT and ACh/ChAT co-localization of immunoreactivity was observed in the bronchial epithelium from COPD. In vitro, CSE stimulation significantly increased mAChRM3, ChAT, and ACh expression and mAChRM3/ChAT and ACh/ChAT co-localization in 16HBE and NHBE, and increased 16HBE proliferation. Cigarette smoke modifies the levels of mAChMR3, ChAT expression, and ACh production in bronchial epithelial cells from COPD patients. Non-neuronal components of cholinergic system may have a role in the mechanism of bronchial epithelial cell proliferation, promoting alteration of normal tissue and of related pulmonary functions. This article is protected by copyright. All rights reserved.
| Original language | English |
|---|---|
| Journal | Journal of Cellular Physiology |
| DOIs | |
| Publication status | Accepted/In press - Nov 27 2017 |
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Cigarette smoke and non-neuronal cholinergic system in the airway epithelium of COPD patients. / Montalbano, Angela Marina; Di Sano, Caterina; Chiappara, Giuseppina; Riccobono, Loredana; Bonanno, Anna; Anzalone, Giulia; Vitulo, Patrizio; Pipitone, Loredana; Gjomarkaj, Mark; Pieper, Michael P; Ricciardolo, Fabio Luigi Massimo; Gagliardo, Rosalia Paola; Profita, Mirella.
In: Journal of Cellular Physiology, 27.11.2017.Research output: Contribution to journal › Article
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TY - JOUR
T1 - Cigarette smoke and non-neuronal cholinergic system in the airway epithelium of COPD patients
AU - Montalbano, Angela Marina
AU - Di Sano, Caterina
AU - Chiappara, Giuseppina
AU - Riccobono, Loredana
AU - Bonanno, Anna
AU - Anzalone, Giulia
AU - Vitulo, Patrizio
AU - Pipitone, Loredana
AU - Gjomarkaj, Mark
AU - Pieper, Michael P
AU - Ricciardolo, Fabio Luigi Massimo
AU - Gagliardo, Rosalia Paola
AU - Profita, Mirella
N1 - This article is protected by copyright. All rights reserved.
PY - 2017/11/27
Y1 - 2017/11/27
N2 - Acetylcholine (ACh), synthesized by Choline Acetyl-Transferase (ChAT), exerts its physiological effects via mAChRM3 in epithelial cells. We hypothesized that cigarette smoke affects ChAT, ACh, and mAChRM3 expression in the airways from COPD patients promoting airway disease. ChAT, ACh, and mAChRM3 were assessed: "ex vivo" in the epithelium from central and distal airways of COPD patients, Healthy Smoker (S) and Healthy Subjects (C), and "in vitro" in bronchial epithelial cells stimulated with cigarette smoke extract (CSE). In central airways, mAChRM3, ChAT, and ACh immunoreactivity was significantly higher in the epithelium from S and COPD than in C subjects. mAChRM3, ChAT, and ACh score of immunoreactivity was high in the metaplastia area of COPD patients. mAChRM3/ChAT and ACh/ChAT co-localization of immunoreactivity was observed in the bronchial epithelium from COPD. In vitro, CSE stimulation significantly increased mAChRM3, ChAT, and ACh expression and mAChRM3/ChAT and ACh/ChAT co-localization in 16HBE and NHBE, and increased 16HBE proliferation. Cigarette smoke modifies the levels of mAChMR3, ChAT expression, and ACh production in bronchial epithelial cells from COPD patients. Non-neuronal components of cholinergic system may have a role in the mechanism of bronchial epithelial cell proliferation, promoting alteration of normal tissue and of related pulmonary functions. This article is protected by copyright. All rights reserved.
AB - Acetylcholine (ACh), synthesized by Choline Acetyl-Transferase (ChAT), exerts its physiological effects via mAChRM3 in epithelial cells. We hypothesized that cigarette smoke affects ChAT, ACh, and mAChRM3 expression in the airways from COPD patients promoting airway disease. ChAT, ACh, and mAChRM3 were assessed: "ex vivo" in the epithelium from central and distal airways of COPD patients, Healthy Smoker (S) and Healthy Subjects (C), and "in vitro" in bronchial epithelial cells stimulated with cigarette smoke extract (CSE). In central airways, mAChRM3, ChAT, and ACh immunoreactivity was significantly higher in the epithelium from S and COPD than in C subjects. mAChRM3, ChAT, and ACh score of immunoreactivity was high in the metaplastia area of COPD patients. mAChRM3/ChAT and ACh/ChAT co-localization of immunoreactivity was observed in the bronchial epithelium from COPD. In vitro, CSE stimulation significantly increased mAChRM3, ChAT, and ACh expression and mAChRM3/ChAT and ACh/ChAT co-localization in 16HBE and NHBE, and increased 16HBE proliferation. Cigarette smoke modifies the levels of mAChMR3, ChAT expression, and ACh production in bronchial epithelial cells from COPD patients. Non-neuronal components of cholinergic system may have a role in the mechanism of bronchial epithelial cell proliferation, promoting alteration of normal tissue and of related pulmonary functions. This article is protected by copyright. All rights reserved.
KW - Journal Article
U2 - 10.1002/jcp.26377
DO - 10.1002/jcp.26377
M3 - Article
JO - Journal of Cellular Physiology
JF - Journal of Cellular Physiology
SN - 1097-4652
ER -