Epidermal growth factor receptor signaling mediates regranulation of rat nasal goblet cells
- Authors
- Lee H.-M.; Malm L.; Dabbagh K.; Dao-Pick T.; Ueki I.F.; Kim S.; Shim J.J.; Nadel J.A.
- Issue Date
- 2001
- Keywords
- Epidermal growth factor receptor cascade; Epidermal growth factor receptor tyrosine kinase activation; Mucin expression; Nasal hypersecretion; Secretory cell growth
- Citation
- Journal of Allergy and Clinical Immunology, v.107, no.6, pp 1046 - 1050
- Pages
- 5
- Indexed
- SCOPUS
- Journal Title
- Journal of Allergy and Clinical Immunology
- Volume
- 107
- Number
- 6
- Start Page
- 1046
- End Page
- 1050
- URI
- https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/22846
- DOI
- 10.1067/mai.2001.115140
- ISSN
- 0091-6749
1097-6825
- Abstract
- Background: Mucus hypersecretion is a common response to inflammation in the lower airways and is a hallmark of chronic rhinitis. Objective: The purpose of this study was to elucidate the mechanisms of regranulation (mucus production) of goblet cells in nasal epitheliumú Methods: Because neutrophils induce an epidermal growth factor (EGFR) cascade, we induced degranulation of goblet cells in rat nasal respiratory epithelium by means of intranasal inhalation of N-formyl-methionyl-leucyl-phenylalanine (fMLP), and we examined regranulation of the goblet cells and the role of EGFR inhibitors and neutrophils in the regranulation process. Results: In the control state Alcian blue/periodic acid-Schiff and mucin MUC5AC staining was present. Degranulation was induced in the nasal septal epithelium 4 hours after intranasal inhalation of fMLP (10-7 mol/L); 48 hours later, goblet-cell regranulation was complete. In the control state EGFR protein staining was absent in the epithelium, but after fMLP-induced degranulation, EGFR protein was expressed. After pretreatment with BIBX1522, a selective EGFR tyrosine kinase inhibitor, fMLP-induced degranulation was unaffected, but goblet-cell regranulation was prevented completely. Conclusion: These data suggest a role for the EGFR cascade in neutrophil-dependent production of goblet-cell mucins. Proving this theory will require the use of selective EGFR inhibitors in clinical studies of nasal hypersecretory states.
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- Appears in
Collections - 2. Clinical Science > Department of Pulmonary, Allergy, and Critical Care Medicine > 1. Journal Articles
- 2. Clinical Science > Department of Otorhinolaryngology-Head and Neck Surgery > 1. Journal Articles
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