Effect of simvastatin on transforming growth factor beta-1-induced myofibroblast differentiation and collagen production in nasal polyp-derived fibroblasts
- Authors
- Park, Il-Ho; Park, Se-Jin; Cho, Jung-Sun; Moon, You-Mi; Moon, Jun-Hyeok; Kim, Tae Hoon; Lee, Sang Hag; Lee, Heung-Man
- Issue Date
- 1월-2012
- Publisher
- OCEAN SIDE PUBLICATIONS INC
- Citation
- AMERICAN JOURNAL OF RHINOLOGY & ALLERGY, v.26, no.1, pp.7 - 11
- Indexed
- SCIE
SCOPUS
- Journal Title
- AMERICAN JOURNAL OF RHINOLOGY & ALLERGY
- Volume
- 26
- Number
- 1
- Start Page
- 7
- End Page
- 11
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/109132
- DOI
- 10.2500/ajra.2012.26.3679
- ISSN
- 1945-8924
- Abstract
- Background: Statins are the most commonly prescribed drugs for the treatment of hypercholesterolemia. Statins exert not only lipid-lowering but also other cellular effects, including antifibrotic properties. The purpose of this study was to determine the effect of simvastatin on transforming growth factor (TGF)-beta-1-induced myofibroblast differentiation and collagen production in nasal polyp-derived fibroblasts (NPDFs) and to verify the mechanism of the effect of simvastatin in TGF-beta-1-induced myofibroblast differentiation in NPDFs. Methods: NPDFs were pretreated with simvastatin with or without mevalonate or Y-27643 for 2 hours before induction by TGF-beta-1. The expression of alpha-smooth muscle actin (SMA) and collagen type IV mRNA was determined by a reverse transcription-polymerase chain reaction, and the expression of alpha-SMA protein was determined by immunofluorescent cytochemical staining. Total soluble collagen production was analyzed by the SirCol collagen dye-binding assay (Biocolor, Belfast, U. K.). Phosphorylation of Smad 2/3 was evaluated by Western blot analysis. Results: In TGF-beta-1-induced NPDFs, simvastatin significantly inhibited the expressions of alpha-SMA and collagen type IV mRNA and reduced alpha-SMA and collagen protein levels. Pretreatment with mevalonate reversed the effect of simvastatin. The expression of alpha-SMA mRNA and protein was significantly decreased by pretreatment with Y-27632. The TGF-beta-1-induced expression of pSmad 2/3 protein was notably decreased by pretreatment with simvastatin. Conclusion: We showed that simvastatin inhibits TGF-beta-1-induced myofibroblast differentiation (expression of alpha-SMA) and collagen production in NPDFs and Rho/Rock and TGF-alpha/Smad signaling is involved as an underlying mechanism. The results of our study suggest that simvastatin is a possible candidate for the suppression of nasal polyp formation. (Am J Rhinol Allergy 26, 7-11, 2012; doi: 10.2500/ajra.2012.26.3679)
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Collections - College of Medicine > Department of Medical Science > 1. Journal Articles
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