Title : Nicotinic Acetylcholine Receptor Subunit α7 Mediates Cigarette Smoke-Induced PD-L1 Expression in Human Bronchial Epithelial Cells.

Pub. Date : 2021 Oct 25

PMID : 34771509






4 Functional Relationships(s)
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1 In the current study, we investigated whether nicotine activation of nicotinic acetylcholine receptor subunit alpha7 (nAChRalpha7, CHRNA7) would induce PD-L1 expression in lung epithelial cells. Nicotine cholinergic receptor nicotinic alpha 7 subunit Homo sapiens
2 In the current study, we investigated whether nicotine activation of nicotinic acetylcholine receptor subunit alpha7 (nAChRalpha7, CHRNA7) would induce PD-L1 expression in lung epithelial cells. Nicotine cholinergic receptor nicotinic alpha 7 subunit Homo sapiens
3 The expression levels of nAChRalpha7 and PD-L1 in eight human bronchial epithelial cell (HBEC) lines were measured after treatment with cigarette smoke extract (CSE) or nicotine derivatives. Nicotine cholinergic receptor nicotinic alpha 7 subunit Homo sapiens
4 In summary, this study demonstrated that the well-known nicotine derivative-activated nAChRalpha7 could induce STAT3/NRF2 pathways and subsequently promote PD-L1 expression in normal lung epithelial cells. Nicotine cholinergic receptor nicotinic alpha 7 subunit Homo sapiens