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Inhibitory Effect of Glucocorticoids on TGF-β1-Mediated Epithelial-to-Mesenchymal Transition of Airway Epithelium Via MAPK and Snail Slug Signaling Pathways
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A3801 - Inhibitory Effect of Glucocorticoids on TGF-β1-Mediated Epithelial-to-Mesenchymal Transition of Airway Epithelium Via MAPK and Snail Slug Signaling Pathways
Author Block: H. Lee1, H. Yang2, S. Lee3, J. Park2, J. Shin1; 1Department of Otorhinolaryngology-Head and Neck Surgery, Korea University, College of Medicine, Seoul, Korea, Republic of, 2Department of Biomedical Science, Korea University, College of Medicine, Seoul, Korea, Republic of, 3Institute for Medical Devices Translation Clinical Trial Support Center, Korea University, College of Medicine, Seoul, Korea, Republic of.
Purpose: 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. Methods: 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. Results: 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. Conclusions: 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.
Author Block: H. Lee1, H. Yang2, S. Lee3, J. Park2, J. Shin1; 1Department of Otorhinolaryngology-Head and Neck Surgery, Korea University, College of Medicine, Seoul, Korea, Republic of, 2Department of Biomedical Science, Korea University, College of Medicine, Seoul, Korea, Republic of, 3Institute for Medical Devices Translation Clinical Trial Support Center, Korea University, College of Medicine, Seoul, Korea, Republic of.
Purpose: 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. Methods: 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. Results: 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. Conclusions: 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.
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