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  • Um, Ji-Young  (7)
  • Medicine  (7)
  • 1
    Online Resource
    Online Resource
    Increased Expression of High-Mobility Group Protein B1 in Chronic Rhinosinusitis
    SAGE Publications ; 2013
    In:  American Journal of Rhinology & Allergy Vol. 27, No. 4 ( 2013-07), p. 278-282
    Details
    In: American Journal of Rhinology & Allergy, SAGE Publications, Vol. 27, No. 4 ( 2013-07), p. 278-282
    Abstract: Chronic rhinosinusitis (CRS) is an inflammation of the sinonasal mucosa and many inflammatory cells and cytokines are involved in its pathogenesis. High-mobility group protein B1 (HMGB1) is a DNA-binding protein that has a proinflammatory function when secreted into extracellular space. The purpose of this study was to evaluate the expression of HMGB1 in paranasal sinus mucosa and to determine the difference of HMGB1 expression between CRS patients and normal controls. Methods Paranasal sinus mucosa was obtained from 10 patients with CRS and 10 patients without CRS. Semiquantitative reverse transcriptase–polymerase chain reaction (RT-PCR), real-time PCR and Western blot analysis were performed to detect mRNA and protein. Sections of the mucosa were immunostained for localization of HMGB1 and image analysis was performed. Results RT-PCR and real-time PCR showed that the expression level of HMGB1 mRNA was significantly increased in the tissues of patients with CRS compared with controls. Western blot analysis showed that the expression level of HMGB1 protein was significantly increased in the tissues of CRS. In immunohistochemical staining, the HMGB1 protein was expressed in epithelial cells and inflammatory cells and the expression intensity of HMGB1 protein was stronger in CRS. Conclusion HMGB1 is increased in the paranasal sinus mucosa of patients with CRS. These results suggest a possible contribution of HMGB1 in the pathophysiology of CRS.
    Type of Medium: Online Resource
    ISSN: 1945-8924 , 1945-8932
    URL: Article
    DOI: 10.2500/ajra.2013.27.3909
    RVK:
    XA 20278
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2013
    detail.hit.zdb_id: 2554548-6
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  • 2
    Online Resource
    Online Resource
    Effect of MeCP2 on TGF- β 1-induced Extracellular Matrix Production in Nasal Polyp-derived Fibroblasts
    SAGE Publications ; 2018
    In:  American Journal of Rhinology & Allergy Vol. 32, No. 4 ( 2018-07), p. 228-235
    Details
    In: American Journal of Rhinology & Allergy, SAGE Publications, Vol. 32, No. 4 ( 2018-07), p. 228-235
    Abstract: Methyl-CpG-binding protein 2 (MeCP2), known as a transcriptional regulator, has been suggested to play an important role in myofibroblast differentiation in the lung. The purpose of this study was to investigate the role of MeCP2 in transforming growth factor (TGF)- β1-induced myofibroblast differentiation and extracellular matrix (ECM) production in nasal polyp-derived fibroblasts (NPDFs). Methods To identify the expression of MeCP2 in nasal polyp tissues, immunohistochemistry staining and Western blot were performed. TGF- β1-induced NPDFs were treated with 5-azacytidine, a DNA methylation inhibitor, and the expression levels of α-SMA and fibronectin were determined by semiquantitative reverse transcription polymerase chain reaction, immunofluorescent staining, and Western blotting. The total soluble collagen was analyzed by the Sircol collagen assay. MeCP2 silenced by MeCP2-specific small interference ( si) RNA was verified by Western blot. Results The expression levels of MeCP2 increased in nasal polyp tissues compared to normal inferior turbinate tissues. 5-Azacytidine significantly inhibited the expression of α-SMA and fibronectin mRNA in a dose-dependent manner. In addition, 5-azacytidine suppressed collagen production and the expression of MeCP2 in the same manner. The expression levels of a-SMA and collagen production were significantly blocked by MeCP2 silencing in TGF- β1-induced NPDFs. Conclusions Our data suggest that MeCP2 plays an essential role in TGF- β1-induced myofibroblast differentiation and ECM production in NPDFs.
    Type of Medium: Online Resource
    ISSN: 1945-8924 , 1945-8932
    URL: Article
    DOI: 10.1177/1945892418770291
    RVK:
    XA 20278
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2018
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  • 3
    Online Resource
    Online Resource
    Effects of Histone Deacetylase Inhibitor on Extracellular Matrix Production in Human Nasal Polyp Organ Cultures
    SAGE Publications ; 2013
    In:  American Journal of Rhinology & Allergy Vol. 27, No. 1 ( 2013-01), p. 18-23
    Details
    In: American Journal of Rhinology & Allergy, SAGE Publications, Vol. 27, No. 1 ( 2013-01), p. 18-23
    Abstract: Nasal polyposis is associated with a chronic inflammatory condition of the sinonasal mucosa and involves myofibroblast differentiation and extracellular matrix (ECM) accumulation. Epigenetic modulation by histone deacetylase (HDAC) inhibitors including trichostatin A (TSA) has been reported to have inhibitory effects on myofibroblast differentiation in lung and renal fibroblasts. The purpose of this study was to investigate the inhibitory effect of TSA on myofibroblast differentiation and ECM production in nasal polyp organ cultures. Methods Nasal polyp tissues from 18 patients were acquired during endoscopic sinus surgery. After organ culture, nasal polyps were stimulated with TGF-beta1 and then treated with TSA. Alpha-smooth muscle actin (α-SMA), fibronectin, and collagen type I expression levels were examined by reverse transcription–polymerase chain reaction (PCR), real-time PCR, Western blot, and immunofluorescent staining. HDAC2, HDAC4, and acetylated H4 expression levels were assayed by Western blot. Cytotoxicity was analyzed by the terminal deoxynucleotidyl transferase biotin–dUTP nick end labeling assay. Results The expression levels of α-SMA, fibronectin, and collagen type 1 were increased in nasal polyp after transforming growth factor (TGF) beta1 treatment. TSA-inhibited TGF-beta1 induced these gene and protein expression levels. Furthermore, TSA suppressed protein expression levels of HDAC2 and HDAC4. However, TSA induced hyperacetylation of histones H4. Treatment with TGF-beta1 with or without TSA did not have cytotoxic effect. Conclusion These findings provide novel insights into the epigenetic regulation in myofibroblast differentiation and ECM production of nasal polyp. TSA could be a candidate of a therapeutic agent for reversing the TGF-beta1–induced ECM synthesis that leads to nasal polyp development.
    Type of Medium: Online Resource
    ISSN: 1945-8924 , 1945-8932
    URL: Article
    DOI: 10.2500/ajra.2013.27.3827
    RVK:
    XA 20278
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2013
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  • 4
    Online Resource
    Online Resource
    Activation Of TLR4 Induces VEGF Expression Via Akt Pathway In Nasal Polyps
    Elsevier BV ; 2014
    In:  Journal of Allergy and Clinical Immunology Vol. 133, No. 2 ( 2014-02), p. AB168-
    Details
    In: Journal of Allergy and Clinical Immunology, Elsevier BV, Vol. 133, No. 2 ( 2014-02), p. AB168-
    Type of Medium: Online Resource
    ISSN: 0091-6749
    URL: Article
    DOI: 10.1016/j.jaci.2013.12.605
    RVK:
    XA 52000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2014
    detail.hit.zdb_id: 2006613-2
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  • 5
    Online Resource
    Online Resource
    Rapamycin Inhibits Transforming Growth Factor Beta 1 Induced Myofibroblast Differentiation via the Phosphorylated-Phosphatidylinositol 3-Kinase Mammalian Target of Rapamycin Signal Pathways in Nasal Polyp–Derived Fibroblasts
    SAGE Publications ; 2016
    In:  American Journal of Rhinology & Allergy Vol. 30, No. 6 ( 2016-11), p. e211-e217
    Details
    In: American Journal of Rhinology & Allergy, SAGE Publications, Vol. 30, No. 6 ( 2016-11), p. e211-e217
    Abstract: Rapamycin has antiproliferative and antifibrogenic effects in vitro and in vivo. The purpose of this study was to evaluate the effects of rapamycin on transforming growth factor (TGF) beta 1 induced myofibroblast differentiation (alpha smooth-muscle actin [SMA]), extracellular matrix production, and collagen contraction in nasal polyp–derived fibroblasts (NPDF). The underlying molecular mechanisms of rapamycin were also determined in NPDFs. Methods NPDFs were grown in culture and transformed into myofibroblasts by using TGF beta 1 (5 ng/mL). For cytotoxicity evaluation, a 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl-tetrazolium bromide assay was used. Expression levels of alpha SMA, phosphorylated phosphatidylinositol 3-kinase (PI3K), and phosphorylated mammalian target of rapamycin (mTOR) were determined by using Western blot, reverse transcription–polymerase chain reaction, and immunofluorescence staining. The total amount of collagen was analyzed by using the Sircol collagen assay, and contractile activity was measured with a collagen gel contraction assay. Silencing mTOR with mTOR-specific small interference RNA was determined by using reverse transcription–polymerase chain reaction. Results Whereas rapamycin (range, 0–400 nM) had no significant cytotoxic effects on TGF beta 1 induced NPDFs, it significantly reduced the expression levels of alpha–SMA in TGF beta 1 induced NPDFs in a dose-dependent manner. TGF beta 1 induced collagen production and collagen contraction were significantly inhibited by rapamycin treatment. Rapamycin also attenuated the TGF beta 1 induced activation of PI3K and mTOR, and its inhibitory effects were similar to those of mTOR silencing and a specific PI3K inhibitor. Conclusions Rapamycin inhibited TGF beta 1 induced myofibroblast differentiation, extracellular matrix production, and collagen contraction through the PI3K/mTOR signal pathways in NPDFs.
    Type of Medium: Online Resource
    ISSN: 1945-8924 , 1945-8932
    URL: Article
    DOI: 10.2500/ajra.2016.30.4389
    RVK:
    XA 20278
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2016
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  • 6
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    Online Resource
    Inhibitory Effect of Prostaglandin E 2 on the Migration of Nasal Fibroblasts
    SAGE Publications ; 2014
    In:  American Journal of Rhinology & Allergy Vol. 28, No. 3 ( 2014-05), p. e120-e124
    Details
    In: American Journal of Rhinology & Allergy, SAGE Publications, Vol. 28, No. 3 ( 2014-05), p. e120-e124
    Abstract: Fibroblast migration is crucial for normal wound repair after sinonasal surgery. Prostaglandin E 2 (PGE 2 ) is a potent inhibitor of fibroblast functions including chemotaxis, proliferation, and matrix production. The purpose of this study was to determine whether PGE 2 affects the migration of nasal fibroblasts and to investigate the mechanism of action of PGE 2 on nasal fibroblasts. Methods Primary cultures of nasal fibroblasts were established from inferior turbinate samples. Fibroblast migration was evaluated with scratch assays. Reverse-transcription polymerase chain reaction was performed for E prostanoid (EP) 1, EP2, EP3, and EP4 receptors. EP receptor–selective agonists and antagonists were used to evaluate receptor functions. Stimulatory G (Gs) proteins were activated to evaluate mechanisms. Intracellular cyclic adenosine monophosphate (cAMP) levels were measured by ELISA, and fibroblast cytoskeletal structures were visualized with immunocytochemistry. Results PGE 2 significantly reduced the migration of nasal fibroblasts. Agonists selective for the EP2 and EP4 receptors significantly reduced the nasal fibroblast migration. Antagonists of the EP2 and EP4 receptors inhibited the effect of PGE 2 on nasal fibroblast migration. Activation of Gs protein and adenyl cyclase reduced nasal fibroblast migration. Conclusion PGE 2 inhibited the migration of nasal fibroblasts via the EP2 and EP4 receptors, and this inhibition was mediated by cAMP elevation. Targeting specific EP receptors could offer therapeutic opportunities for conditions such as delayed wound healing after nasal surgery.
    Type of Medium: Online Resource
    ISSN: 1945-8924 , 1945-8932
    URL: Article
    DOI: 10.2500/ajra.2014.28.4039
    RVK:
    XA 20278
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2014
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  • 7
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    Online Resource
    Wogonin Inhibits Transforming Growth Factor β1–induced Extracellular Matrix Production via the p38/activator Protein 1 Signaling Pathway in Nasal Polyp–derived Fibroblasts
    SAGE Publications ; 2016
    In:  American Journal of Rhinology & Allergy Vol. 30, No. 4 ( 2016-07), p. e128-e133
    Details
    In: American Journal of Rhinology & Allergy, SAGE Publications, Vol. 30, No. 4 ( 2016-07), p. e128-e133
    Abstract: 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) β1–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-β1–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 α-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 μM) had no significant cytotoxic effects on TGF-β1–induced NPDFs. Migration of NPDFs was significantly inhibited by wogonin treatment. The expression levels of α-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-β1–induced NPDFs. Conclusion These results indicated that wogonin may inhibit TGF-β–induced myofibroblast differentiation, extracellular matrix production, migration, and collagen contraction through the p38/activator protein-1 pathway in NPDFs.
    Type of Medium: Online Resource
    ISSN: 1945-8924 , 1945-8932
    URL: Article
    DOI: 10.2500/ajra.2016.30.4329
    RVK:
    XA 20278
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2016
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