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(American Journal of Pathology. 2006;168:55-68.)
© 2006 American Society for Investigative Pathology

{alpha}3{alpha}5ß2-Nicotinic Acetylcholine Receptor Contributes to the Wound Repair of the Respiratory Epithelium by Modulating Intracellular Calcium in Migrating Cells

Jean-Marie Tournier*, Kamel Maouche*, Christelle Coraux*, Jean-Marie Zahm*, Isabelle Cloëz-Tayarani{dagger}, Béatrice Nawrocki-Raby*, Arnaud Bonnomet*, Henriette Burlet*, François Lebargy*{ddagger}, Myriam Polette*§ and Philippe Birembaut*§

From INSERM UMRS-514,* IFR53, Université de Reims, Reims; Unité de Biologie Cellulaire,§ Laboratoire Pol Bouin, and Service de Pneumologie,{ddagger} CHU de Reims, Reims; and Unité Récepteurs et Cognition,{dagger} CNRS URA-2182, Institut Pasteur Paris, Paris, France

Nicotinic acetylcholine receptors (nAChRs), present in human bronchial epithelial cells (HBECs), have been shown in vitro to modulate cell shape. Because cell spreading and migration are important mechanisms involved in the repair of the bronchial epithelium, we investigated the potential role of nAChRs in the wound repair of the bronchial epithelium. In vivo and in vitro, {alpha}3{alpha}5ß2-nAChRs accumulated in migrating HBECs involved in repairing a wound, whereas {alpha}7-nAChRs were predominantly observed in stationary confluent cells. Wound repair was improved in the presence of nAChR agonists, nicotine, and acetylcholine, and delayed in the presence of {alpha}3ß2 neuronal nAChR antagonists, mecamylamine, {alpha}-conotoxin MII, and {kappa}-bungarotoxin; {alpha}-bungarotoxin, an antagonist of {alpha}7-nAChR, had no effect. Addition of nicotine to a repairing wound resulted in a dose-dependent transient increase of intracellular calcium in migrating cells that line the wound edge. Mecamylamine and {kappa}-bungarotoxin inhibited both the cell-migration speed and the nicotine-induced intracellular calcium increase in wound-repairing migrating cells in vitro. On the contrary {alpha}-bungarotoxin had no significant effect on migrating cells. These results suggest that {alpha}3{alpha}5ß2-nAChRs actively contribute to the wound repair process of the respiratory epithelium by modulating intracellular calcium in wound-repairing migrating cells.




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E. Puchelle, J.-M. Zahm, J.-M. Tournier, and C. Coraux
Airway Epithelial Repair, Regeneration, and Remodeling after Injury in Chronic Obstructive Pulmonary Disease
Proceedings of the ATS, November 1, 2006; 3(8): 726 - 733.
[Abstract] [Full Text] [PDF]


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Copyright © 2006 by the American Society for Investigative Pathology.