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Background  Nicotinic acetylcholine receptors (nAChRs) are ligand-gated ion channels comprised of five similar subunits that influence signal transduction and cell turnover. α 5  is a structural subunit detected in many non-neuronal tissues; however, its function during pulmonary development is unknown.    Results  α 5  was assessed by immunohistochemistry and RT-PCR in mouse lungs from embryonic day (E)13.5 to post-natal day (PN)20. From E13.5 to E18.5, α 5  expression was primarily observed in primitive airway epithelial cells while mesenchymal expression was faint and sporadic. α 5  expression was detected throughout the proximal lung at PN1 and extensively expressed in the peripheral lung at PN4, an early stage of murine alveologenesis. An interesting shift occurred wherein α 5  expression was almost undetectable in the proximal lung from PN4-PN10, but significant localization was again observed at PN20. Transcriptional control of α 5  was determined by assessing the activity of reporters containing 2.0-kb and 850-bp of the mouse α 5  promoter. Because perinatal expression of α 5  was abundant in bronchiolar and alveolar epithelium, we assessed transcriptional control of α 5  in Beas2B cells, a human bronchiolar epithelial cell line, and A-549 cells, an alveolar type II cell-like human epithelial cell line. Thyroid Transcription Factor-1 (TTF-1), a key transcription regulator of pulmonary morphogenesis, significantly increased α 5  transcription by acting on both the 2.0-kb and 850-bp α 5  promoters. Site-directed mutagenesis revealed that TTF-1 activated α 5  transcription by binding specific TTF-1 response elements. Exogenous TTF-1 also significantly induced α 5  transcription.    Conclusions  These data demonstrate that α 5  is specifically controlled in a temporal and spatial manner during pulmonary morphogenesis. Ongoing research may demonstrate that precise regulation of α 5  is important during normal organogenesis and misexpression correlates with tobacco related lung disease.

TTF-1 regulates α5 nicotinic acetylcholine receptor (nAChR) subunits in proximal and distal lung epithelium