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1 Centre de recherche , Centre hospitalier de l, Montreal, Canada; Departement de Medecine , Universite de Montreal, Montreal, Canada
2 Centre de recherche, Centre hospitalier de l'Universite de Montreal (CHUM) _ Hotel-Dieu, Montreal, Canada
3 Centre de recherche, Centre hospitalier de l, Montreal, Canada; Departement de Medecine, Universite de Montreal, Montreal, Canada
4 GEPROM, Departement de Physiologie, Universite de Montreal, Montreal, Canada
5 Centre de recherche , Centre hospitalier de l, Montreal, Canada; Departement de Medecine , Universite de Montreal, Montreal, Canada; GEPROM, Departement de Physiologie , Universite de Montreal, Montreal, Canada
* To whom correspondence should be addressed. E-mail: emmanuelle.brochiero{at}umontreal.ca.
Several respiratory diseases are associated with extensive damage of lung epithelia, and the regulatory mechanisms involved in their regeneration are not clearly defined. Growth factors released by epithelial cells or fibroblasts from injured lungs are important regulators of alveolar repair by stimulating cell motility, proliferation and differentiation. In addition, K+ channels regulate cell proliferation/migration and are coupled with growth factor signaling in several tissues. We decided to explore the hypothesis, never investigated before, that K+ could play a prominent role in alveolar repair. We employed a model of mechanical wounding of rat alveolar type II epithelia, in primary culture, to study their response to injury. Wound-healing was suppressed by half upon EGF titration with EGF-Ab or erbB1/erbB2 tyrosine-kinase inhibition with AG1478/AG825. The addition of exogenous EGF slightly stimulated the alveolar wound-healing and enhanced, by up to 5 times, alveolar cell migration measured in a Boyden-type chamber. Conditioned medium collected from injured alveolar monolayers also stimulated cell migration; this effect was abolished in the presence of EGF-Ab. The impact of K+ channel modulators was examined in basal and EGF-stimulated conditions. Wound-healing was stimulated by pinacidil, a KATP activator, which also increased cell migration, by 2-fold, in basal conditions and potentiated the stimulatory effect of EGF. KATP or KvLQT1 inhibitors (glibenclamide, clofilium) reduced EGF-stimulated wound-healing, cell migration and proliferation. Finally, EGF stimulated KATP and KvLQT1 currents and channel expression. In summary, stimulation of K+ channels through autocrine activation of EGF receptors could play a crucial role in lung epithelia repair processes.
This article has been cited by other articles:
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  O. Bardou, N. T. N. Trinh, and E. Brochiero Molecular diversity and function of K+ channels in airway and alveolar epithelial cells Am J Physiol Lung Cell Mol Physiol, February 1, 2009; 296(2): L145 - L155. [Abstract] [Full Text] [PDF]
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N. T. N. Trinh, A. Prive, E. Maille, J. Noel, and E. Brochiero EGF and K+ channel activity control normal and cystic fibrosis bronchial epithelia repair Am J Physiol Lung Cell Mol Physiol, November 1, 2008; 295(5): L866 - L880. [Abstract] [Full Text] [PDF]
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 A. Schwab, P. Hanley, A. Fabian, and C. Stock Potassium Channels Keep Mobile Cells on the Go Physiology, August 1, 2008; 23(4): 212 - 220. [Abstract] [Full Text] [PDF]
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