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Vol. 54, Issue 5, 779-788, November 1998
Department of Biochemistry, University of Minnesota, St. Paul,
Minnesota 55108 (A.D.J.M., P.I.K., R.M.H., D.N., K.M., B.M.C.-F.),
Department of Pharmacology, University of Minnesota, Minneapolis,
Minnesota 55455 (B.M.C.-F.),
Department of Pharmacology and
Experimental Therapeutics, University of Maryland School of
Medicine, Baltimore, Maryland 21201 (E.F.R.P., W.S.C., E.X.A.), and
Institute of Biophysics, Carlos Chagas Filho, and Department of Basic
and Clinical Pharmacology, Federal University of Rio de Janeiro, Rio de
Janeiro, RJ 21944, Brazil (E.X.A.)
We demonstrated previously that human skin keratinocytes express
acetylcholine receptors (AChRs) sensitive to acetylcholine and
nicotine, which regulate cell adhesion and motility. We demonstrate here that human and rodent bronchial epithelial cells (BECs) express AChRs similar to those expressed by keratinocytes and by some neurons.
Patch-clamp experiments demonstrated that the BEC AChRs are functional,
and they are activated by acetylcholine and nicotine. They are blocked
by 
-bungarotoxin, a specific antagonist of the AChR isotypes
expressed by neurons in ganglia. Their ion-gating properties are
consistent with those of AChR isotypes expressed in ganglia, formed by
3, 5, and 
2 or 4 subunits. Reverse transcription-polymerase chain reaction and in situ hybridization experiments
demonstrated the presence in BECs of mRNA transcripts for all those
AChR subunits, both in cell cultures and in tissue sections, whereas we
could not detect transcripts for the 2, 4, 6, and 3 AChR
subunits. The expression of 3 and 5 proteins in BEC in
vivo was verified by the binding of subunit-specific antibodies
to sections of trachea. Mecamylamine and -bungarotoxin, which are
cholinergic antagonists able to block the ganglionic 3 AChRs, caused
a reversible change of the cell shape of cultured, confluent human
BECs. This resulted in a reduction of the area covered by the cell and
in cell/cell detachment. The presence of AChRs sensitive to
nicotine on the lining of the airways raises the possibility that the
high concentrations of nicotine resulting from tobacco smoking will
cause an abnormal activation, a desensitization, or both of the
bronchial AChRs. This may mediate or facilitate some of the toxic
effects of cigarette smoking in the respiratory system.
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