American journal of rhinology & allergy · 2009
Expression of glutaredoxin-1 in nasal polyps and airway epithelial cells.
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Woo Hyun-Jae, Bae Chang Hoon, Song Si-Youn, Kim Yong-Woon, Lee Heung-Man, Kim Yong-Dae
Аннотация
BACKGROUND: Glutaredoxins (GRX)-1 is glutathione-dependent oxidoreductase. However, the role of these enzymes remains unknown in airway inflammatory diseases. Therefore, we aimed to establish the expression pattern of GRX-1 in the nasal polyps (NPs) and to assess the regulatory mechanisms associated with GRX-1 expression in interleukin (IL)-1 beta-treated airway epithelial cells.
METHODS: The expression of GRX-1 in NPs and normal nasal mucosa were analyzed by reverse-transcription polymerase chain reaction and immunohistochemical staining. IL-1 beta-induced reactive oxygen species (ROS) formation and GRX-1 expression in the airway epithelial cells was determined by flow cytometry and immunoassay.
RESULTS: The expression level of GRX-1 in NPs was significantly higher than in the normal nasal mucosa (p < 0.05). GRX-1 was highly expressed in the surface epithelial cells and the submucosal glandular cells in the NPs. IL-1 beta increased the intracellular ROS formation and GRX-1 expression in airway epithelial cells. The inhibition of IL-1 beta-induced ROS production by N-acetyl-cystein, an ROS scavenger, reduced GRX-1 expression. Diphenyleneiodonium and apocynin, NADPH oxidase inhibitors, did not abolish IL-1 beta-induced ROS formation and GRX-1 expression, whereas budesonide attenuated it.
CONCLUSION: High GRX-1 expression in NPs might be a primary defense against chronic inflammatory oxidative stress in nasal mucosa. IL-1 beta-induced up-regulation of GRX-1 in airway epithelial cells is probably mediated by ROS. Glucocorticoids can regulate IL-1 beta-induced ROS formation and GRX-1 expression.
METHODS: The expression of GRX-1 in NPs and normal nasal mucosa were analyzed by reverse-transcription polymerase chain reaction and immunohistochemical staining. IL-1 beta-induced reactive oxygen species (ROS) formation and GRX-1 expression in the airway epithelial cells was determined by flow cytometry and immunoassay.
RESULTS: The expression level of GRX-1 in NPs was significantly higher than in the normal nasal mucosa (p < 0.05). GRX-1 was highly expressed in the surface epithelial cells and the submucosal glandular cells in the NPs. IL-1 beta increased the intracellular ROS formation and GRX-1 expression in airway epithelial cells. The inhibition of IL-1 beta-induced ROS production by N-acetyl-cystein, an ROS scavenger, reduced GRX-1 expression. Diphenyleneiodonium and apocynin, NADPH oxidase inhibitors, did not abolish IL-1 beta-induced ROS formation and GRX-1 expression, whereas budesonide attenuated it.
CONCLUSION: High GRX-1 expression in NPs might be a primary defense against chronic inflammatory oxidative stress in nasal mucosa. IL-1 beta-induced up-regulation of GRX-1 in airway epithelial cells is probably mediated by ROS. Glucocorticoids can regulate IL-1 beta-induced ROS formation and GRX-1 expression.