Human and Rodent Bronchial Epithelial Cells Express Functional Nicotinic Acetylcholine Receptors

摘要: We demonstrated previously that human skin keratinocytes express acetylcholine receptors (AChRs) sensitive to and nicotine, which regulate cell adhesion motility. demonstrate here rodent bronchial epithelial cells (BECs) AChRs similar those expressed by some neurons. Patch-clamp experiments the BEC are functional, they activated nicotine. They blocked κ-bungarotoxin, a specific antagonist of AChR isotypes neurons in ganglia. Their ion-gating properties consistent with ganglia, formed α3, α5, β2 or β4 subunits. Reverse transcription-polymerase chain reaction situ hybridization presence BECs mRNA transcripts for all subunits, both cultures tissue sections, whereas we could not detect α2, α4, α6, β3 The expression α3 α5 proteins vivo was verified binding subunit-specific antibodies sections trachea. Mecamylamine cholinergic antagonists able block ganglionic AChRs, caused reversible change shape cultured, confluent BECs. This resulted reduction area covered cell/cell detachment. nicotine on lining airways raises possibility high concentrations resulting from tobacco smoking will cause an abnormal activation, desensitization, AChRs. may mediate facilitate toxic effects cigarette respiratory system.