Wogonin inhibits transforming growth factor 1-induced extracellular matrix production via the p38/activator protein 1 signaling pathway in nasal polyp-derived fibroblasts

Nam Hyoung Ryu, Jae Min Shin, Ji Young Um, Il Ho Park, Heung Man Lee

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Background: Wogonin has been shown to have antifibrotic and anti-inflammatory effects in the lower airway. The purpose of this study was to evaluate the effects of wogonin on transforming growth factor (TGF) 1-induced myofibroblast differentiation, extracellular matrix production, migration, and collagen contraction, and to determine the molecular mechanisms of wogonin in nasal polyp-derived fibroblasts (NPDF). Methods: NPDFs were isolated from nasal polyps from eight patients. TGF-1-induced NPDFs were treated with wogonin. Cytotoxicity was evaluated by using a 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl-tetrazolium bromide assay. Fibroblast migration was evaluated with transwell and scratch migration assays. The expression levels of -smooth muscle actin, fibronectin, phosphorylated-p38, and c-Fos were determined by Western blot and/or reverse transcription-polymerase chain reaction. The total collagen amount was analyzed with the Sircol collagen assay, and contractile activity was measured by a collagen gel contraction assay. Results: Wogonin (0-60 M) had no significant cytotoxic effects on TGF-1-induced NPDFs. Migration of NPDFs was significantly inhibited by wogonin treatment. The expression levels of -smooth muscle actin and fibronectin were significantly reduced in wogonin-treated NPDFs. Collagen production and contraction were also significantly decreased by wogonin treatment. Wogonin markedly inhibited activation of the p38/activator protein 1 pathway in TGF-1-induced NPDFs. Conclusion: These results indicated that wogonin may inhibit TGF-1-induced myofibroblast differentiation, extracellular matrix production, migration, and collagen contraction through the p38/activator protein-1 pathway in NPDFs.

Original languageEnglish
Pages (from-to)e128-e133
JournalAmerican Journal of Rhinology and Allergy
Volume30
Issue number4
DOIs
Publication statusPublished - 2016 Jul 1

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Nasal Polyps
Transcription Factor AP-1
Transforming Growth Factors
Extracellular Matrix
Fibroblasts
Collagen
Myofibroblasts
Fibronectins
Smooth Muscle
Actins
wogonin
Bromides
Reverse Transcription
Anti-Inflammatory Agents
Western Blotting
Gels

ASJC Scopus subject areas

  • Immunology and Allergy
  • Otorhinolaryngology

Cite this

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title = "Wogonin inhibits transforming growth factor 1-induced extracellular matrix production via the p38/activator protein 1 signaling pathway in nasal polyp-derived fibroblasts",
abstract = "Background: Wogonin has been shown to have antifibrotic and anti-inflammatory effects in the lower airway. The purpose of this study was to evaluate the effects of wogonin on transforming growth factor (TGF) 1-induced myofibroblast differentiation, extracellular matrix production, migration, and collagen contraction, and to determine the molecular mechanisms of wogonin in nasal polyp-derived fibroblasts (NPDF). Methods: NPDFs were isolated from nasal polyps from eight patients. TGF-1-induced NPDFs were treated with wogonin. Cytotoxicity was evaluated by using a 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl-tetrazolium bromide assay. Fibroblast migration was evaluated with transwell and scratch migration assays. The expression levels of -smooth muscle actin, fibronectin, phosphorylated-p38, and c-Fos were determined by Western blot and/or reverse transcription-polymerase chain reaction. The total collagen amount was analyzed with the Sircol collagen assay, and contractile activity was measured by a collagen gel contraction assay. Results: Wogonin (0-60 M) had no significant cytotoxic effects on TGF-1-induced NPDFs. Migration of NPDFs was significantly inhibited by wogonin treatment. The expression levels of -smooth muscle actin and fibronectin were significantly reduced in wogonin-treated NPDFs. Collagen production and contraction were also significantly decreased by wogonin treatment. Wogonin markedly inhibited activation of the p38/activator protein 1 pathway in TGF-1-induced NPDFs. Conclusion: These results indicated that wogonin may inhibit TGF-1-induced myofibroblast differentiation, extracellular matrix production, migration, and collagen contraction through the p38/activator protein-1 pathway in NPDFs.",
author = "Ryu, {Nam Hyoung} and Shin, {Jae Min} and Um, {Ji Young} and Park, {Il Ho} and Lee, {Heung Man}",
year = "2016",
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language = "English",
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pages = "e128--e133",
journal = "American Journal of Rhinology and Allergy",
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TY - JOUR

T1 - Wogonin inhibits transforming growth factor 1-induced extracellular matrix production via the p38/activator protein 1 signaling pathway in nasal polyp-derived fibroblasts

AU - Ryu, Nam Hyoung

AU - Shin, Jae Min

AU - Um, Ji Young

AU - Park, Il Ho

AU - Lee, Heung Man

PY - 2016/7/1

Y1 - 2016/7/1

N2 - Background: Wogonin has been shown to have antifibrotic and anti-inflammatory effects in the lower airway. The purpose of this study was to evaluate the effects of wogonin on transforming growth factor (TGF) 1-induced myofibroblast differentiation, extracellular matrix production, migration, and collagen contraction, and to determine the molecular mechanisms of wogonin in nasal polyp-derived fibroblasts (NPDF). Methods: NPDFs were isolated from nasal polyps from eight patients. TGF-1-induced NPDFs were treated with wogonin. Cytotoxicity was evaluated by using a 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl-tetrazolium bromide assay. Fibroblast migration was evaluated with transwell and scratch migration assays. The expression levels of -smooth muscle actin, fibronectin, phosphorylated-p38, and c-Fos were determined by Western blot and/or reverse transcription-polymerase chain reaction. The total collagen amount was analyzed with the Sircol collagen assay, and contractile activity was measured by a collagen gel contraction assay. Results: Wogonin (0-60 M) had no significant cytotoxic effects on TGF-1-induced NPDFs. Migration of NPDFs was significantly inhibited by wogonin treatment. The expression levels of -smooth muscle actin and fibronectin were significantly reduced in wogonin-treated NPDFs. Collagen production and contraction were also significantly decreased by wogonin treatment. Wogonin markedly inhibited activation of the p38/activator protein 1 pathway in TGF-1-induced NPDFs. Conclusion: These results indicated that wogonin may inhibit TGF-1-induced myofibroblast differentiation, extracellular matrix production, migration, and collagen contraction through the p38/activator protein-1 pathway in NPDFs.

AB - Background: Wogonin has been shown to have antifibrotic and anti-inflammatory effects in the lower airway. The purpose of this study was to evaluate the effects of wogonin on transforming growth factor (TGF) 1-induced myofibroblast differentiation, extracellular matrix production, migration, and collagen contraction, and to determine the molecular mechanisms of wogonin in nasal polyp-derived fibroblasts (NPDF). Methods: NPDFs were isolated from nasal polyps from eight patients. TGF-1-induced NPDFs were treated with wogonin. Cytotoxicity was evaluated by using a 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl-tetrazolium bromide assay. Fibroblast migration was evaluated with transwell and scratch migration assays. The expression levels of -smooth muscle actin, fibronectin, phosphorylated-p38, and c-Fos were determined by Western blot and/or reverse transcription-polymerase chain reaction. The total collagen amount was analyzed with the Sircol collagen assay, and contractile activity was measured by a collagen gel contraction assay. Results: Wogonin (0-60 M) had no significant cytotoxic effects on TGF-1-induced NPDFs. Migration of NPDFs was significantly inhibited by wogonin treatment. The expression levels of -smooth muscle actin and fibronectin were significantly reduced in wogonin-treated NPDFs. Collagen production and contraction were also significantly decreased by wogonin treatment. Wogonin markedly inhibited activation of the p38/activator protein 1 pathway in TGF-1-induced NPDFs. Conclusion: These results indicated that wogonin may inhibit TGF-1-induced myofibroblast differentiation, extracellular matrix production, migration, and collagen contraction through the p38/activator protein-1 pathway in NPDFs.

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U2 - 10.2500/ajra.2016.30.4329

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SP - e128-e133

JO - American Journal of Rhinology and Allergy

JF - American Journal of Rhinology and Allergy

SN - 1945-8924

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