Decreased S100A9 Expression Promoted Rat Airway Smooth Muscle Cell Proliferation by Stimulating ROS Generation and Inhibiting p38 MAPK

Background. Asthma is a disease with a core abnormality in airway smooth muscle function, and the proliferation of airway smooth muscle cells (ASMCs) plays a pivotal role in asthma airway remodeling. Our previous study showed that S100A9 (S100 calcium-binding protein A9; 400 and 800 ng/mL) significa...

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Bibliographic Details
Published in:Canadian respiratory journal 2016-01, Vol.2016 (2016), p.1-7
Main Authors: Yang, Yong Qing, Wang, Yu, Xu, Yu-Dong, Duan, Ting-Ting, Han, Xiao-Jie, Yin, Lei-Miao, Ulloa, Luis
Format: Article
Language:English
Subjects:
Analysis
Animals
Asthma
Asthma - metabolism
Asthma - physiopathology
Calgranulin B - physiology
Cell growth
Cell Proliferation
Cells, Cultured
Chinese medicine
Extracellular signal-regulated kinases
Gene expression
Growth factors
Inflammation
Kinases
MAP Kinase Signaling System
Mortality
Myocytes, Smooth Muscle - physiology
Neutrophils
Pathogenesis
Phosphorylation
Physiological aspects
Proteins
Rats
Reactive oxygen species
Reactive Oxygen Species - metabolism
Risk factors
Signal transduction
Smooth muscle
Studies
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Summary:Background. Asthma is a disease with a core abnormality in airway smooth muscle function, and the proliferation of airway smooth muscle cells (ASMCs) plays a pivotal role in asthma airway remodeling. Our previous study showed that S100A9 (S100 calcium-binding protein A9; 400 and 800 ng/mL) significantly inhibited rat ASMCs proliferation at 48 h, and 50–800 ng/mL S100A9 (50, 100, 200, 400, and 800 ng/mL) also induced a lasting effect by significantly inhibiting rat ASMCs proliferation at 72 h in a dose-dependent manner. However, the intracellular effects of S100A9 on ASMCs proliferation remain unknown. Methods. Rat ASMCs with stable S100A9 knockdown were generated using short hairpin RNA. The effects of decreased S100A9 expression on cellular proliferation, the production of reactive oxygen species (ROS), and p38 MAPK pathway protein expression were examined. Results. Decreased intracellular S100A9 expression significantly promoted platelet-derived growth factor-induced rat ASMCs proliferation and increased ROS production. The antioxidative agent N-acetylcysteine significantly inhibited rat ASMCs proliferation. Western blot results showed that the decreased intracellular S100A9 expression significantly inhibited p38 MAPK phosphorylation. Conclusion. Decreased S100A9 expression promoted rat ASMCs proliferation by stimulating ROS generation and inhibiting p38 MAPK. Our study may provide novel insights into the regulation of asthma airway remodeling.
ISSN:1198-2241
1916-7245
DOI:10.1155/2016/1462563