Author/Authors :
Yin, Lei-Miao Laboratory of Molecular Biology - Shanghai Research Institute of Acupuncture and Meridian - Yue Yang Hospital - Shanghai University of Traditional Chinese Medicine, Shanghai, China , Han, Xiao-Jie Laboratory of Molecular Biology - Shanghai Research Institute of Acupuncture and Meridian - Yue Yang Hospital - Shanghai University of Traditional Chinese Medicine, Shanghai, China , Duan, Ting-Ting Laboratory of Molecular Biology - Shanghai Research Institute of Acupuncture and Meridian - Yue Yang Hospital - Shanghai University of Traditional Chinese Medicine, Shanghai, China , Xu, Yu-Dong Laboratory of Molecular Biology - Shanghai Research Institute of Acupuncture and Meridian - Yue Yang Hospital - Shanghai University of Traditional Chinese Medicine, Shanghai, China , Wang, Yu Laboratory of Molecular Biology - Shanghai Research Institute of Acupuncture and Meridian - Yue Yang Hospital - Shanghai University of Traditional Chinese Medicine, Shanghai, China , Ulloa, Luis Laboratory of Molecular Biology - Shanghai Research Institute of Acupuncture and Meridian - Yue Yang Hospital - Shanghai University of Traditional Chinese Medicine, Shanghai, China , Yang, Yong-Qing Laboratory of Molecular Biology - Shanghai Research Institute of Acupuncture and Meridian - Yue Yang Hospital - Shanghai University of Traditional Chinese Medicine, Shanghai, China
Abstract :
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 calciumbinding 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 dosedependent 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.
Keywords :
Muscle Cell , Proliferation , Stimulating ROS Generation , Inhibiting p38 MAPK
