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Am J Physiol Lung Cell Mol Physiol 274: L165-L170, 1998;
1040-0605/98 $5.00
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Vol. 274, Issue 1, L165-L170, January 1998

RAPID COMMUNICATION
Nicotine stimulates branching and expression of SP-A and SP-C mRNAs in embryonic mouse lung culture

Carol W. Wuenschell1, Jingsong Zhao1, J. Denise Tefft1, and David Warburton1,2

1 Center for Craniofacial Molecular Biology, School of Dentistry, University of Southern California, Los Angeles 90033; and 2 Developmental Biology Program, Department of Surgery, Childrens Hospital Los Angeles Research Institute, Los Angeles, California 90027

Although the effects of maternal smoking on fetal growth and viability are overwhelmingly negative, there is a paradoxical enhancement of lung maturation as evidenced, in part, by a lower incidence of respiratory distress syndrome in infants of smoking mothers. Other epidemiologic and experimental evidence further support the view that a tobacco smoke constituent, possibly nicotine, affects the development of the lung in utero. We are studying the direct effects of nicotine on murine lung development using a serumless organ culture system. We have found that embryonic lungs explanted at 11 days gestation showed a 32% increase in branching after 4 days in culture in the presence of 1 µM nicotine and 7- to 15-fold increases in mRNAs encoding surfactant proteins A and C after 11 days. The effect of nicotine exposure on surfactant gene expression is apparently mediated by nicotinic acetylcholine receptors because it was blocked by D-tubocurarine. The nicotine-induced stimulation of surfactant gene expression could, in part, account for the effect of maternal smoking on the incidence of respiratory distress syndrome.

surfactant protein A; surfactant protein C; messenger ribonucleic acid; respiratory distress syndrome; nicotinic acetylcholine receptors; branching morphogenesis; lung development


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