Chronic rhinosinusitis with nasal polyps (CRSwNP) is characterized by significant tissue remodeling, in which Epithelial–mesenchymal transition (EMT) plays a pivotal role in this process. Autophagy, a cellular degradation mechanism crucial for maintaining cellular homeostasis, may also contribute to EMT in CRSwNP.
Objectives
To investigate the role of autophagy in EMT during CRSwNP.
Methods
Tissue specimens were obtained from control subjects and patients with CRSwNP. The expression levels of human neutrophil elastase (HNE), Transforming growth factor-β1 (TGF-β1), the autophagic protein LC3, and EMT-related markers (E-cadherin, N-cadherin, and vimentin) were detected using immunohistochemistry and Western blotting. The expression characteristics of TGF-β1 in CRSwNP and their relationship with autophagy caused by HNE was assessed by in-vitro culture of the human nasal epithelial cell line RPMI-2650 treated with human recombinant HNE.
Results
Patients with CRSwNP had more protein expression of TGF-β1, LC3, N-cadherin, and vimentin, whereas the expression of E-cadherin was significantly decreased (P < .05). Treatment of nasal epithelial cells with recombinant HNE also induced the upregulation of TGF-β1, LC3, N-cadherin and Vimentin, while reducing E-cadherin levels (P < .05). Alternatively, treatment of nasal epithelial cells with an autophagy inhibitor or a TGF-β1 inhibitor mitigated EMT.
Conclusion
HNE induced EMT by activating the autophagy in CRSwNP and TGF-β1 also played an important role in this process.
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