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  • 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
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  • 2
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    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
    Vitamin D attenuates myofibroblast differentiation and extracellular matrix accumulation in nasal polyp-derived fibroblasts through smad2/3 signaling pathway
    Springer Science and Business Media LLC ; 2017
    In:  Scientific Reports Vol. 7, No. 1 ( 2017-08-04)
    Details
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 7, No. 1 ( 2017-08-04)
    Abstract: To investigate the potential role of vitamin D (1,25(OH) 2 D 3 ) in preventing the development of nasal polyps, we examined the effect of vitamin D on myofibroblast differentiation and extracellular matrix (ECM) production in TGF-β1-induced nasal polyp-derived fibroblasts (NPDFs) and elucidated the mechanisms underlying its inhibitory effect. 1,25(OH) 2 D 3 significantly reduced expression levels of α-SMA, a myofibroblast marker, and fibronectin, a representative ECM component, in a dose-dependent manner in TGF-β1-induced NPDFs. 1,25(OH) 2 D 3 suppressed activated Smad2/3 in time-course. Up-regulation of α-SMA, fibronectin and phosphorylation of Smad2/3 by TGF-β1 was unaffected by 1,25(OH) 2 D 3 in NPDFs after vitamin D receptor-specific siRNA transfection. We confirmed that the Smad2/3-specific inhibitor SIS3 inactivated Smad2/3 and reduced α-SMA and fibronectin expression. Furthermore, acetylation of histone H3 was compromised by 1,25(OH) 2 D 3, leading to inhibition of collagen 1A1 , collagen 1A2 and α-SMA gene expression. Treatment with 1,25(OH) 2 D 3 also significantly suppressed TGF-β1-enhanced contractility and motility in a contraction assay and Transwell migration assay. Finally, 1,25(OH) 2 D 3 had a similar effect in ex vivo organ cultures of nasal polyps. Taken together, our results suggest that 1,25(OH) 2 D 3 might be an effective therapy for nasal polyps by reducing myofibroblast differentiation and ECM production mediated by Smad2/3-dependent TGF-β1 signaling pathways in NPDFs.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    URL: Article
    DOI: 10.1038/s41598-017-07561-6
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2017
    detail.hit.zdb_id: 2615211-3
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  • 4
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    Glucocorticoids ameliorate TGF-β1-mediated epithelial-to-mesenchymal transition of airway epithelium through MAPK and Snail/Slug signaling pathways
    Springer Science and Business Media LLC ; 2017
    In:  Scientific Reports Vol. 7, No. 1 ( 2017-06-14)
    Details
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 7, No. 1 ( 2017-06-14)
    Abstract: Chronic rhinosinusitis with nasal polyps (CRSwNP) is closely associated with tissue remodeling. Epithelial-to-mesenchymal transition (EMT), a process of tissue remodeling, can be a therapeutic target of CRSwNP. Glucocorticoids are a type of steroid hormone that is used primarily in medical therapy for patients with CRSwNP; however, their effects on EMT in the airway epithelium remain unknown. To investigate the effects of dexamethasone and fluticasone propionate, a class of glucocorticoids, on transforming growth factor-β1 (TGF-β1) -induced EMT, we used A549 cells, human primary nasal epithelial cells (hPNECs) and ex vivo organ culture of the inferior turbinate. TGF-β1 induced changes in cell morphology, suppressed the expression of E-cadherin and enhanced the expression of a-smooth muscle actin, vimentin and fibronectin in A549 cells. However, glucocorticoids inhibited EMT, migration and invasion enhancement by TGF-β1. We found that the induction of phosphorylated ERK, p38 and the activity of Snail and Slug transcription factors by TGF-β1 were suppressed by glucocorticoids. Glucocorticoids also had a similar effect in hPNECs and ex vivo organ cultures of the inferior turbinate. These findings suggest that glucocorticoids might be a useful therapy for preventing tissue remodeling by blocking the EMT initiated by TGF-β1-induced MAPK and Snail/Slug signaling pathways in CRSwNP.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    URL: Article
    DOI: 10.1038/s41598-017-02358-z
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2017
    detail.hit.zdb_id: 2615211-3
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  • 5
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    Online Resource
    Effect of Doxycycline on Transforming Growth Factor-Beta-1–Induced Matrix Metalloproteinase 2 Expression, Migration, and Collagen Contraction in Nasal Polyp–Derived Fibroblasts
    SAGE Publications ; 2016
    In:  American Journal of Rhinology & Allergy Vol. 30, No. 6 ( 2016-11), p. 385-390
    Details
    In: American Journal of Rhinology & Allergy, SAGE Publications, Vol. 30, No. 6 ( 2016-11), p. 385-390
    Abstract: It is well known that doxycycline has antibacterial and anti-inflammatory effects. In this study, we aimed to investigate the effects of doxycycline on the transforming growth factor (TGF) beta 1–induced matrix metalloproteinase (MMP) 2 expression, migration, and collagen contraction, and to determine its molecular mechanism on nasal polyp–derived fibroblasts (NPDF). Methods NPDFs were isolated from the nasal polyps of six patients. Doxycycline was used to pretreat TGF-beta-1–induced NPDFs and ex vivo organ cultures of nasal polyps. Cytotoxicity was evaluated by using a 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl-tetrazolium bromide assay. Smad2/3 is one of the major transcription factors of TGF-beta signaling. The expression levels of MMP2 and Smad2/3 were measured by using Western blotting, reverse transcription-polymerase chain reaction, and immunofluorescence staining. The enzymic activity of MMP2 was analyzed by using gelatin zymography. Fibroblast migration was evaluated by using transwell migration assays. Contractile activity was measured by a collagen gel contraction assay. Results The expression level of MMP2 in nasal polyp tissues increased in comparison with inferior turbinate tissues. TGF-beta-1–induced NPDFs were not affected by doxycycline (0–40 μg/mh). The expression levels of MMP2 and activation of Smad2/3 in TGF-beta-1–induced NPDFs and in organ cultures of nasal polyps were significantly downregulated with doxycycline pretreatment. Doxycycline also reduced TGF-beta-1–induced fibroblast migration and collagen contraction in NPDFs. Conclusion Doxycycline inhibited TGF-beta-1–induced MMP2 expression, migration, and collagen contraction via the Smad2/3 signal pathways in NPDFs.
    Type of Medium: Online Resource
    ISSN: 1945-8924 , 1945-8932
    URL: Article
    DOI: 10.2500/ajra.2016.30.4381
    RVK:
    XA 20278
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2016
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  • 6
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    Online Resource
    Effect of Doxycycline on Epithelial-Mesenchymal Transition via the p38/Smad Pathway in Respiratory Epithelial Cells
    SAGE Publications ; 2017
    In:  American Journal of Rhinology & Allergy Vol. 31, No. 2 ( 2017-03), p. 71-77
    Details
    In: American Journal of Rhinology & Allergy, SAGE Publications, Vol. 31, No. 2 ( 2017-03), p. 71-77
    Abstract: Doxycycline has antibacterial and anti-inflammatory effects, and it also suppresses collagen biosynthesis. This study aimed to confirm the effects and mechanism of doxycycline on transforming growth factor (TGF) beta 1 induced epithelial-mesenchymal transition and cell migration in A549 and primary nasal epithelial cells. Methods A 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide assay and phalloidin-fluorescein isothiocyanate staining were used to evaluate cytotoxicity and cellular morphologic changes. Western blot and immunofluorescence staining were used to determine the expression levels of E-cadherin, vimentin, alpha-smooth muscle actin, fibronectin, phosphorylated Smad2/3, and mitogen-activated protein kinases. Scratch and transwell migration assays were used to assess cellular migration ability. Results Doxycycline (0-10 μg/mL) had no significant cytotoxic effects in A549 and primary nasal epithelial cells. Increased expression of mesenchymal markers, including vimentin, alpha-smooth muscle actin, and fibronectin in TGF beta 1 induced A549 cells were downregulated by doxycycline treatment. In contrast, E-cadherin expression was upregulated in TGF beta 1 induced A549 cells. An in vitro cell migration assay showed that doxycycline also inhibited the ability of TGF beta 1 induced migration. Doxycycline treatment suppressed the activation of Smad2/3 and p38, whereas its inhibitory effects were similar to each element-specific inhibitor in A549 and primary nasal epithelial cells. Conclusion Doxycycline inhibited TGF beta 1 induced epithelial-to-mesenchymal transition and migration by targeting Smad2/3 and p38 signal pathways in respiratory epithelial cells.
    Type of Medium: Online Resource
    ISSN: 1945-8924 , 1945-8932
    URL: Article
    DOI: 10.2500/ajra.2017.31.4410
    RVK:
    XA 20278
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2017
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  • 7
    Online Resource
    Online Resource
    Role of Adenosine Monophosphate-Activated Protein Kinase on Cell Migration, Matrix Contraction, and Matrix Metalloproteinase-1 and Matrix Metalloproteinase-2 Production in Nasal Polyp–Derived Fibroblasts
    SAGE Publications ; 2017
    In:  American Journal of Rhinology & Allergy Vol. 31, No. 6 ( 2017-11), p. 357-363
    Details
    In: American Journal of Rhinology & Allergy, SAGE Publications, Vol. 31, No. 6 ( 2017-11), p. 357-363
    Abstract: Activation of adenosine monophosphate-activated protein kinase (AMPK) by metformin, as a master regulator of metabolism, is involved in airway tissue remodeling. Here, we investigated the physical role of AMPK on cell migration, matrix contraction, and the production of matrix metalloproteinases (MMP) in nasal polyp–derived fibroblasts (NPDF). Methods Primary NPDFs from six patients with chronic rhinosinusitis and nasal polyps were isolated and cultured. To assess the effect of AMPK on fibroblast migration, we conducted scratch and migration assays in NPDF treated with metformin and/or compound C. A collagen gel contraction assay measured activity of contractile. MMP expression was measured with reverse transcription-polymerase chain reaction, Western blot, and zymography. To evaluate for specific AMPK action, we examined by AMPK small interfering RNA. Results Metformin, an activator of AMPK, significantly inhibited cell migration in NPDFs in a dose-dependent manner. Compound C, an inhibitor of AMPK, partially reversed the inhibitory effect of metformin. Metformin also significantly decreased contractile activity, with a concomitant reduction in the production of MMP-1 and MMP-2 but not of MMP-9. Specific silencing that targeted AMPK resulted in the enhancement of mobility and contractility and in the production of MMP-1 and MMP-2. Conclusion AMPK played an important role in regulating cell migration, matrix contraction, and MMP production in NPDFs, which provided data that AMPK activator might be a therapeutic target for the prevention of tissue remodeling in nasal polyps.
    Type of Medium: Online Resource
    ISSN: 1945-8924 , 1945-8932
    URL: Article
    DOI: 10.2500/ajra.2017.31.4477
    RVK:
    XA 20278
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2017
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  • 8
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    Diesel Exhaust Particles Upregulate Interleukins IL-6 and IL-8 in Nasal Fibroblasts
    Public Library of Science (PLoS) ; 2016
    In:  PLOS ONE Vol. 11, No. 6 ( 2016-6-13), p. e0157058-
    Details
    In: PLOS ONE, Public Library of Science (PLoS), Vol. 11, No. 6 ( 2016-6-13), p. e0157058-
    Type of Medium: Online Resource
    ISSN: 1932-6203
    URL: Article
    URL: Article
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    URL: Article
    URL: Article
    DOI: 10.1371/journal.pone.0157058
    DOI: 10.1371/journal.pone.0157058.g001
    DOI: 10.1371/journal.pone.0157058.g002
    DOI: 10.1371/journal.pone.0157058.g003
    DOI: 10.1371/journal.pone.0157058.g004
    DOI: 10.1371/journal.pone.0157058.g005
    DOI: 10.1371/journal.pone.0157058.g006
    DOI: 10.1371/journal.pone.0157058.g007
    Language: English
    Publisher: Public Library of Science (PLoS)
    Publication Date: 2016
    detail.hit.zdb_id: 2267670-3
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  • 9
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    Cigarette Smoke Extract Stimulates MMP-2 Production in Nasal Fibroblasts via ROS/PI3K, Akt, and NF-κB Signaling Pathways
    MDPI AG ; 2020
    In:  Antioxidants Vol. 9, No. 8 ( 2020-08-12), p. 739-
    Details
    In: Antioxidants, MDPI AG, Vol. 9, No. 8 ( 2020-08-12), p. 739-
    Abstract: Cigarette smoke exposure has been shown to be associated with chronic rhinosinusitis and tissue remodeling. The present study aimed to investigate the effects of cigarette smoke extract (CSE) on matrix metalloproteinase (MMP) and tissue inhibitor of metalloproteinase (TIMP) production in nasal fibroblasts and to determine the underlying molecular mechanisms. Primary nasal fibroblasts from six patients were isolated and cultured. After the exposure of fibroblasts to CSE, the expression levels of MMP-2, MMP-9, TIMP-1, and TIMP-2 were measured by real-time PCR, ELISA, and immunofluorescence staining. The enzymatic activities of MMP-2 and MMP-9 were measured by gelatin zymography. Reactive oxygen species (ROS) production was analyzed using dichloro-dihydro-fluorescein diacetate and Amplex Red assays. PI3K/Akt phosphorylation and NF-κB activation were determined by Western blotting and luciferase assay. CSE significantly increased MMP-2 expression and inhibited TIMP-2 expression but did not affect MMP-9 and TIMP-1 expression. Furthermore, CSE significantly induced ROS production. However, treatment with ROS scavengers, specific PI3K/Akt inhibitors, NF-κB inhibitor, and glucocorticosteroids significantly decreased MMP-2 expression and increased TIMP-2 expression. Our results suggest that steroids inhibit CSE-regulated MMP-2 and TIMP-2 production and activation through the ROS/ PI3K, Akt, and NF-κB signaling pathways in nasal fibroblasts. CSE may contribute to the pathogenesis of chronic rhinosinusitis by regulating MMP-2 and TIMP-2 expression.
    Type of Medium: Online Resource
    ISSN: 2076-3921
    URL: Article
    DOI: 10.3390/antiox9080739
    Language: English
    Publisher: MDPI AG
    Publication Date: 2020
    detail.hit.zdb_id: 2704216-9
    SSG: 15,3
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  • 10
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    Efficacy of hyaluronic acid and hydroxyethyl starch in preventing adhesion following endoscopic sinus surgery
    Springer Science and Business Media LLC ; 2017
    In:  European Archives of Oto-Rhino-Laryngology Vol. 274, No. 10 ( 2017-10), p. 3643-3649
    Details
    In: European Archives of Oto-Rhino-Laryngology, Springer Science and Business Media LLC, Vol. 274, No. 10 ( 2017-10), p. 3643-3649
    Type of Medium: Online Resource
    ISSN: 0937-4477 , 1434-4726
    URL: Article
    DOI: 10.1007/s00405-017-4669-6
    RVK:
    XA 26650
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2017
    detail.hit.zdb_id: 1459042-6
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