KMID : 0900220200270010034
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´ëÇѺñ°úÇÐȸÁö 2020 Volume.27 No. 1 p.34 ~ p.40
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Effect of Tobacco-specific Nitrosamines on MUC5AC Expression in Human Airway Epithelial Cells
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Kwak So-Young
Choi Yoon-Seok Na Hyung-Gyun Bae Chang-Hoon Song Si-Youn Kim Yong-Dae
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Abstract
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Background and Objectives: Nicotine is oxidized into tobacco-specific nitrosamines (TSNAs; NAB, NAT, NNN, NNAL, NNK) at high temperature and high pressure. TSNAs are associated with airway diseases characterized by mucus hypersecretion as a major pathophysiologic phenomenon. The aim of study is to investigate the effect of TSNAs on mucin overexpression and its molecular mechanism in human airway epithelial cells.
Materials and Method: The cytotoxicity of TSNAs was evaluated using EX-Cytox and inverted microscopy. The mRNA and protein levels of MUC5AC and MUC5B were measured using real-time PCR and ELISA.
Results: NAB, NNN, NNAL, and NNK did not affect cell viability. NAT did not affect cell viability up to a concentration of 100 ¥ìM in human airway epithelial cells. NAT, NNN, NNAL, and NNK significantly induced MUC5AC expression, but not MUC5B expression. NAB did not affect the expression of MUC5AC and MUC5B. Propranolol (a ¥â-adrenergic receptor antagonist) inhibited NAT, NNN, NNAL, and NNK-induced MUC5AC expression, whereas ¥á-bungarotoxin (an ¥á7-nicotinic acetylcholine receptor antagonist) only inhibited NNN- and NNK-induced MUC5AC expression.
Conclusion: These results suggested that NAT, NNN, NNAL, and NNK induce MUC5AC expression through ¥â-adrenergic receptor and/or ¥á7-nicotinic acetylcholine receptor in human airway epithelial cells, which may be involved in mucus hypersecretion in inflammatory airway diseases.
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KEYWORD
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Tobacco-specific nitrosamines, MUC5AC, Human airway epithelial cell
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