Expression of glutaredoxin-1 in nasal polyps and airway epithelial cells

Hyun Jae Woo, Chang Hoon Bae, Si Youn Song, Yong Woon Kim, Heung Man Lee, Yong Dae Kim

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

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)-1beta-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-1beta-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-1beta increased the intracellular ROS formation and GRX-1 expression in airway epithelial cells. The inhibition of IL-1beta-induced ROS production by N-acetyl-cystein, an ROS scavenger, reduced GRX-1 expression. Diphenyleneiodonium and apocynin, NADPH oxidase inhibitors, did not abolish IL-1beta-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-1beta-induced up-regulation of GRX-1 in airway epithelial cells is probably mediated by ROS. Glucocorticoids can regulate IL-1beta-induced ROS formation and GRX-1 expression.

Original languageEnglish
Pages (from-to)288-293
Number of pages6
JournalAmerican Journal of Rhinology and Allergy
Volume23
Issue number3
DOIs
Publication statusPublished - 2009 Sep 25

Fingerprint

Glutaredoxins
Nasal Polyps
Epithelial Cells
Interleukin-1beta
Reactive Oxygen Species
Nasal Mucosa
Budesonide
NADPH Oxidase
Immunoassay

Keywords

  • Airway epithelial cells
  • Glucocorticoids
  • Glutaredoxin-1
  • Interleukin-1β
  • Nasal polyps
  • Oxidative stress
  • Reactive oxygen species

ASJC Scopus subject areas

  • Otorhinolaryngology
  • Immunology and Allergy

Cite this

Expression of glutaredoxin-1 in nasal polyps and airway epithelial cells. / Woo, Hyun Jae; Bae, Chang Hoon; Song, Si Youn; Kim, Yong Woon; Lee, Heung Man; Kim, Yong Dae.

In: American Journal of Rhinology and Allergy, Vol. 23, No. 3, 25.09.2009, p. 288-293.

Research output: Contribution to journalArticle

Woo, Hyun Jae ; Bae, Chang Hoon ; Song, Si Youn ; Kim, Yong Woon ; Lee, Heung Man ; Kim, Yong Dae. / Expression of glutaredoxin-1 in nasal polyps and airway epithelial cells. In: American Journal of Rhinology and Allergy. 2009 ; Vol. 23, No. 3. pp. 288-293.
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abstract = "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)-1beta-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-1beta-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-1beta increased the intracellular ROS formation and GRX-1 expression in airway epithelial cells. The inhibition of IL-1beta-induced ROS production by N-acetyl-cystein, an ROS scavenger, reduced GRX-1 expression. Diphenyleneiodonium and apocynin, NADPH oxidase inhibitors, did not abolish IL-1beta-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-1beta-induced up-regulation of GRX-1 in airway epithelial cells is probably mediated by ROS. Glucocorticoids can regulate IL-1beta-induced ROS formation and GRX-1 expression.",
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AU - Woo, Hyun Jae

AU - Bae, Chang Hoon

AU - Song, Si Youn

AU - Kim, Yong Woon

AU - Lee, Heung Man

AU - Kim, Yong Dae

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N2 - 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)-1beta-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-1beta-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-1beta increased the intracellular ROS formation and GRX-1 expression in airway epithelial cells. The inhibition of IL-1beta-induced ROS production by N-acetyl-cystein, an ROS scavenger, reduced GRX-1 expression. Diphenyleneiodonium and apocynin, NADPH oxidase inhibitors, did not abolish IL-1beta-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-1beta-induced up-regulation of GRX-1 in airway epithelial cells is probably mediated by ROS. Glucocorticoids can regulate IL-1beta-induced ROS formation and GRX-1 expression.

AB - 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)-1beta-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-1beta-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-1beta increased the intracellular ROS formation and GRX-1 expression in airway epithelial cells. The inhibition of IL-1beta-induced ROS production by N-acetyl-cystein, an ROS scavenger, reduced GRX-1 expression. Diphenyleneiodonium and apocynin, NADPH oxidase inhibitors, did not abolish IL-1beta-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-1beta-induced up-regulation of GRX-1 in airway epithelial cells is probably mediated by ROS. Glucocorticoids can regulate IL-1beta-induced ROS formation and GRX-1 expression.

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KW - Glucocorticoids

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KW - Interleukin-1β

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KW - Oxidative stress

KW - Reactive oxygen species

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