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KMID : 0361020210640120887
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Korean Journal of Otolaryngology - Head and Neck Surgery
2021 Volume.64 No. 12 p.887 ~ p.895
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Peroxiredoxin 2 Inhibits Lipopolysaccharide Induced Mucin Expression and Reactive Oxygen Species Production in Human Airway Epithelial Cells
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Kim Joon-Hee
Jo Soo-Yeon
Lee Sang-Jae
Yoo Gi-Moon
Na Hyung-Gyun
Choi Yoon-Seok
Bae Chang-Hoon
Song Si-Youn
Kim Yong-Dae
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Abstract
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Background and Objectives : Peroxiredoxin (Prx) is an antioxidant enzyme involved in signalingpathway. Prx2 is the most abundant in mammalian gray matter neurons and has protectiverole under oxidative stress. MUC5AC and MUC5B are typical mucin genes in human airwayepithelial cells. Even if free radicals play a key role in chronic respiratory inflammatorydiseases, the effects of the Prx2 on mucin expression and oxidative stress are not clearly known.
The purpose of this study is to investigate the effect of Prx2 on lipopolysaccharide (LPS)-inducedMUC5AC/5B expression and reactive oxygen species (ROS) in human airway epithelialcells.
Subjects and Method : In NCI-H292 cells and human nasal epithelial cells, the effects ofPrx2 on LPS-induced MUC5AC/5B expression and ROS production were investigated usingreverse transcriptase-polymerase chain reaction, real-time polymerase chain reaction, enzymelinked immunosorbent assay (ELISA) and flow cytometry analysis.
Results : MUC5AC, MUC5B mRNA expression and protein production were increased byLPS. ROS production was also increased by LPS. Prx2 suppressed the LPS-induced MUC5ACmRNA expression and protein production as well as ROS production. However, Prx2 did notinhibit MUC5B mRNA expression and protein production. N-acetylcysteine, diphenyleneiodonium,and apocynin also inhibited LPS-induced ROS production.
Conclusion : These results may show that Prx2 suppresses LPS-induced MUC5AC expressionvia ROS in human airway epithelial cells.
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KEYWORD
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Human airway epithelial cells, Mucin, MUC5AC, Peroxiredoxin 2, Reactive oxygen species
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