Peroxiredoxin 2 Inhibits Lipopolysaccharide Induced Mucin Expression and Reactive Oxygen Species Production in Human Airway Epithelial Cells
10.3342/kjorl-hns.2021.00171
- Author:
Joon-Hee KIM
1
;
Sooyeon JO
;
Sangjae LEE
;
Gi Moon YOO
;
Hyung Gyun NA
;
Yoon Seok CHOI
;
Chang Hoon BAE
;
Si-Youn SONG
;
Yong-Dae KIM
Author Information
1. Department of Otorhinolaryngology-Head and Neck Surgery, College of Medicine, Yeungnam University, Daegu, Korea
- Publication Type:Original Article
- From:Korean Journal of Otolaryngology - Head and Neck Surgery
2021;64(12):887-895
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Background and Objectives:Peroxiredoxin (Prx) is an antioxidant enzyme involved in signaling pathway. Prx2 is the most abundant in mammalian gray matter neurons and has protective role under oxidative stress. MUC5AC and MUC5B are typical mucin genes in human airway epithelial cells. Even if free radicals play a key role in chronic respiratory inflammatory diseases, 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)-induced MUC5AC/5B expression and reactive oxygen species (ROS) in human airway epithelial cells.Subjects and Method In NCI-H292 cells and human nasal epithelial cells, the effects of Prx2 on LPS-induced MUC5AC/5B expression and ROS production were investigated using reverse transcriptase-polymerase chain reaction, real-time polymerase chain reaction, enzyme linked immunosorbent assay (ELISA) and flow cytometry analysis.
Results:MUC5AC, MUC5B mRNA expression and protein production were increased by LPS. ROS production was also increased by LPS. Prx2 suppressed the LPS-induced MUC5AC mRNA expression and protein production as well as ROS production. However, Prx2 did not inhibit 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 expression via ROS in human airway epithelial cells.
