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|Title:||Down-regulation of EMP1 is associated with epithelial hyperplasia and metaplasia in nasal polyps|
Epithelial hyperplasia or metaplasia
|Source:||Yu, X.M., Li, C.W., Li, Y.Y., Liu, J., Lin, Z.B., Li, T.Y., Zhao, L., Pan, X.L., Shi, L., Wang, D.Y. (2013-11). Down-regulation of EMP1 is associated with epithelial hyperplasia and metaplasia in nasal polyps. Histopathology 63 (5) : 686-695. ScholarBank@NUS Repository. https://doi.org/10.1111/his.12211|
|Abstract:||Aims: The aim of this study was to assess protein and mRNA expression of epithelial membrane protein 1 (EMP1) in the nasal mucosa of patients with nasal polyps (NP), and to determine what changes occur in response to glucocorticosteroid (GC) treatment. Methods and results: NP tissue was obtained from 55 patients, 18 of whom were treated with nasal GCs (i.e. these 18 patients had NP biopsies taken before and after treatment). Biopsies of inferior turbinate mucosa from 30 healthy subjects were used as controls. Quantitative PCR and immunohistochemistry were performed to determine the expression levels of EMP1. EMP1 mRNA expression was significantly lower (2.77-fold) in tissues from NP patients before GC treatment when compared to controls, but was increased in these patients after GC treatment. EMP1 staining in nasal epithelium co-localized with both basal (p63+) and differentiated (CK18+) epithelial cells. Their immunoreactivity was significantly greater in controls than NP patients. EMP1 mRNA levels were lower in the epithelium with severe hyperplasia (1.79-fold) or with metaplasia (1.85-fold) as compared to those with mild to moderate hyperplasia or non-metaplastic epithelium, respectively. Positive correlations between EMP1 and other epithelial cell-related gene (e.g. JUN, PTGS2, AREG etc.) mRNAs were observed. Conclusions: EMP1 could be a biomarker for aberrant epithelial remodelling and metaplasia in chronic inflammatory upper airway mucosa (e.g. NP). © 2013 John Wiley & Sons Ltd635 November 2013 10.1111/his.12211 Original Article Original Articles © 2013 John Wiley & Sons Ltd.|
|Appears in Collections:||Staff Publications|
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