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Originally published online as doi:10.2353/ajpath.2009.090212 on October 1, 2009

Published online before print October 1, 2009
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(American Journal of Pathology. 2009;175:1868-1882.)
© 2009 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2009.090212

{alpha}7 Nicotinic Acetylcholine Receptor Regulates Airway Epithelium Differentiation by Controlling Basal Cell Proliferation

Kamel Maouche*{dagger}{ddagger}, Myriam Polette*{dagger}§, Thomas Jolly*{dagger}, Kahina Medjber*{dagger}, Isabelle Cloëz-Tayarani{ddagger}, Jean-Pierre Changeux{ddagger}, Henriette Burlet*{dagger}, Christine Terryn{dagger}, Christelle Coraux*{dagger}, Jean-Marie Zahm*{dagger}, Philippe Birembaut*{dagger}§ and Jean-Marie Tournier*{dagger}

From the Institut National de la Santé et de la Recherche Médicale (INSERM) U903,* Reims; IFR53, UMR-S903,{dagger} Université de Reims Champagne Ardenne, Reims; the Département de Neuroscience,{ddagger} Institut pasteur, Paris; and the Centre Hospitalier Universitiare Reims,§ Hôpital Maison Blanche, Laboratoire Pol Bouin, Reims, France

Airway epithelial basal cells are known to be critical for regenerating injured epithelium and maintaining tissue homeostasis. Recent evidence suggests that the {alpha}7 nicotinic acetylcholine receptor (nAChR), which is highly permeable to Ca2+, is involved in lung morphogenesis. Here, we have investigated the potential role of the {alpha}7 nAChR in the regulation of airway epithelial basal cell proliferation and the differentiation of the human airway epithelium. In vivo during fetal development and in vitro during the regeneration of the human airway epithelium, {alpha}7 nAChR expression coincides with epithelium differentiation. Inactivating {alpha}7 nAChR function in vitro increases cell proliferation during the initial steps of the epithelium regeneration, leading to epithelial alterations such as basal cell hyperplasia and squamous metaplasia, remodeling observed in many bronchopulmonary diseases. The regeneration of the airway epithelium after injury in {alpha}7–/– mice is delayed and characterized by a transient hyperplasia of basal cells. Moreover, 1-year-old {alpha}7–/– mice more frequently present basal cells hyperplasia. Modulating nAChR function or expression shows that only {alpha}7 nAChR, as opposed to heteropentameric {alpha}xβy nAChRs, controls the proliferation of human airway epithelial basal cells. These findings suggest that {alpha}7 nAChR is a key regulator of the plasticity of the human airway epithelium by controlling basal cell proliferation and differentiation pathway and is involved in airway remodeling during bronchopulmonary diseases.


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