Expression of SLURP-1, an endogenous α7 nicotinic acetylcholine receptor allosteric ligand, in murine bronchial epithelial cells

2009 ◽  
Vol 87 (12) ◽  
pp. 2740-2747 ◽  
Author(s):  
Kazuhide Horiguchi ◽  
Satomi Horiguchi ◽  
Naomi Yamashita ◽  
Kaoru Irie ◽  
Junya Masuda ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Acetylcholine Receptor ◽  
Nicotinic Acetylcholine Receptor ◽  
Bronchial Epithelial Cells ◽  
Α7 Nicotinic Acetylcholine Receptor ◽  
Nicotinic Acetylcholine ◽  
Bronchial Epithelial

scholarly journals Nicotinic Acetylcholine Receptor Subunit α7 Mediates Cigarette Smoke-Induced PD-L1 Expression in Human Bronchial Epithelial Cells

Cancers ◽  
2021 ◽  
Vol 13 (21) ◽  
pp. 5345
Author(s):  
Hoi-Hin Kwok ◽  
Boning Gao ◽  
Koon-Ho Chan ◽  
Mary Sau-Man Ip ◽  
John Dorrance Minna ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Acetylcholine Receptor ◽  
Cigarette Smoke ◽  
Nicotinic Acetylcholine Receptor ◽  
Lung Epithelial Cells ◽  
Receptor Subunit ◽  
Nicotinic Acetylcholine ◽  
Bronchial Epithelial ◽  
Lung Epithelial ◽  
Nicotine Derivatives

Tobacco smoking is the top risk factor for lung cancer development. Nicotine in cigarettes can induce addiction, and its derivatives become potent carcinogens after metabolic activation and activate oncogenic signaling in lung epithelial cells through their expressed nicotinic acetylcholine receptors (nAChRs). However, the effects of smoking on the tumor immune microenvironment are under investigation. In the current study, we investigated whether nicotine activation of nicotinic acetylcholine receptor subunit α7 (nAChRα7, CHRNA7) would induce PD-L1 expression in lung epithelial cells. The expression levels of nAChRα7 and PD-L1 in eight human bronchial epithelial cell (HBEC) lines were measured after treatment with cigarette smoke extract (CSE) or nicotine derivatives. The results showed that PD-L1 expression levels increased in HBECs after exposure to CSE or nicotine derivatives. This induction of PD-L1 expression could be diminished by treatment with CHRNA7 small-interfering RNA, and the relevant signaling was mediated via STAT3 phosphorylation and NRF2 expression. In summary, this study demonstrated that the well-known nicotine derivative-activated nAChRα7 could induce STAT3/NRF2 pathways and subsequently promote PD-L1 expression in normal lung epithelial cells. This information provides mechanistic insight into cigarette smoke-induced immune evasion in lung epithelial cells.

APN1125: A clinical stage α7 nicotinic acetylcholine receptor partial agonist

2015 ◽  
Vol 97 (4) ◽  
pp. 636 ◽  
Author(s):  
Gerald Koelsch ◽  
Michael J. Detke ◽  
Karen E. Stevens ◽  
Leonard T. Meltzer ◽  
Alvin V. Terry ◽  
...  
Keyword(s):  
Acetylcholine Receptor ◽  
Nicotinic Acetylcholine Receptor ◽  
Partial Agonist ◽  
Clinical Stage ◽  
Α7 Nicotinic Acetylcholine Receptor ◽  
Nicotinic Acetylcholine
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