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Am J Physiol Lung Cell Mol Physiol (June 1, 2007). doi:10.1152/ajplung.00038.2007
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Submitted on January 25, 2007
Accepted on May 31, 2007

Nicotine alters lung branching morphogenesis through the {alpha}7 nicotinic acetylcholine receptor

Cherry Wongtrakool1*, Susanne Roser-Page2, Hilda N Rivera2, and Jesse Roman3

1 Pulmonary, Emory University School of Medicine, Atlanta, Georgia, United States
2 Pulmonary, Atlanta VA Medical Center, Decatur, Georgia, United States
3 Pulmonary, Emory University School of Medicine, Atlanta, Georgia, United States; Pulmonary, Atlanta VA Medical Center, Decatur, Georgia, United States

* To whom correspondence should be addressed. E-mail: cwongtr{at}emory.edu.

There is abundant epidemiologic data linking prenatal environmental tobacco smoke with childhood asthma and wheezing, but the underlying molecular and physiologic mechanisms that occur in utero to explain this link remain unelucidated. Several studies suggest that nicotine, which traverses the placenta, is a causative agent. Therefore, we studied the effects of nicotine on lung branching morphogenesis using embryonic murine lung explants. We found that the expression of {alpha}7 nicotinic acetylcholine receptors, which mediate many of the biological effects of nicotine, is highest in pseudoglandular stage lungs when compared to later stages. We then studied the effects of nicotine in the explant model and found that nicotine stimulated lung branching in a dose-dependent fashion. {alpha}-bungarotoxin, an antagonist of {alpha}7 nicotinic acetylcholine receptors, blocked the stimulatory effect of nicotine, whereas GTS-21, a specific agonist, stimulated branching thereby mimicking the effects of nicotine. Explants deficient in {alpha}7 nicotinic acetylcholine receptors did not respond to nicotine. Nicotine also stimulated the growth of the explant. Altogether, these studies suggest that nicotine stimulates lung branching morphogenesis through {alpha}7 nicotinic acetylcholine receptors and may contribute to dysanaptic lung growth which, in turn, may predispose the host to airways disease in the postnatal period.




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