The expression of 11 beta-hydroxysteroid dehydrogenase type 1 and 2 in nasal polyp-derived epithelial cells and its possible contribution to glucocorticoid activation in nasal polyp
- Authors
- Kook, Jin Ho; Kim, Hyun Jin; Kim, Kyung Won; Park, Se Jin; Kim, Tae Hoon; Lim, Sae Hee; Kang, Sung Hoon; Lee, Sang Hag
- Issue Date
- Jul-2015
- Publisher
- OCEAN SIDE PUBLICATIONS INC
- Citation
- AMERICAN JOURNAL OF RHINOLOGY & ALLERGY, v.29, no.4, pp.246 - 250
- Indexed
- SCIE
SCOPUS
- Journal Title
- AMERICAN JOURNAL OF RHINOLOGY & ALLERGY
- Volume
- 29
- Number
- 4
- Start Page
- 246
- End Page
- 250
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/93147
- DOI
- 10.2500/ajra.2015.29.4185
- ISSN
- 1945-8924
- Abstract
- Background: The actions of glucocorticoids in target tissues depend on the local metabolism of glucocorticoids catalyzed by 11 beta hydroxysteroid dehydrogenase (HSD) 1 and 2. Glucocorticoids are the most effective anti-inflammatory drugs in the treatment of nasal polyps. However, the mechanisms that underlie the anti-inflammatory effects are unclear. Objective: The present study analyzed the expression of 11 beta-HSD1, 11 beta-HSD2, and steroidogenic enzymes (cytochrome P450, family 11, subfamily B, polypeptide 1 [CYP11B1]; cytochrome P450, family 11, subfamily A, polypeptide 1 [CYP11A1]) in nasal polyp tissues, and endogenous cortisol levels in nasal polyp-derived epithelial cells. Methods: The expression levels and distribution pattern of 11 beta-HSD1, 11 beta-HSD2, CYP11B1, and CYP11A1 were determined in nasal polyp tissues or nasal polyp-derived epithelial cells by using real-time polymerase chain reaction, Western blot, and immunohistochemistry testing. The expression levels of cortisol by using enzyme-linked immunosorbent assay were determined in cultured polyp-derived epithelial cells treated with adrenocorticotrophic hormone (ACTH), 11 beta-HSD1 inhibitor, or small interfering ribonucleic acid technique. The effect of glucocorticoids on the expression levels of these enzymes was investigated in cultured cells. Results: Expressed in nasal polyp tissues and nasal polyp-derived epithelial cells were 11 beta-HSD1, 11 beta-HSD2, CYP11B1, and CYP11A1. Cortisol production in cultured epithelial cells was decreased in cells treated with 11 beta-HSD1 small interfering ribonucleic acid or inhibitor, compared with nontreated cells. Cultured cells treated with adrenocorticotropic hormone induced increased cortisol production. 11 beta-HSD1 expression levels were upregulated in cells treated with glucocorticoid. Conclusions: Analysis of these results indicated that 11 beta-HSD1 expressed in polyp-derived epithelial cells may be involved in the anti-inflammatory function of glucocorticoid in the treatment of nasal polyps, which contributes to increased levels of endogenous cortisol.
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Collections - Graduate School > Department of Biomedical Sciences > 1. Journal Articles
- College of Medicine > Department of Medical Science > 1. Journal Articles
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