Effect of epidermal growth factor receptor on airway remodeling in asthmatic mice and its mechanism.
- Author:
Xiao-Hui LI
1
;
Bin LUAN
Author Information
- Publication Type:Journal Article
- MeSH: Airway Remodeling; Animals; Asthma; drug therapy; pathology; Heparin-binding EGF-like Growth Factor; Immunohistochemistry; Intercellular Signaling Peptides and Proteins; analysis; genetics; Male; Mice; Quinazolines; Receptor, Epidermal Growth Factor; antagonists & inhibitors; genetics; physiology; Tyrphostins; therapeutic use
- From: Chinese Journal of Contemporary Pediatrics 2010;12(2):137-140
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the relationship of airway remodeling with epidermal growth factor receptor (EGFR) and heparin-binding epidermal growth factor-like growth factor (HB-EGF) levels in asthmatic mice and the effect of EGFR tyrosine kinase inhibitor (AG1478) on airway remodeling.
METHODSTwenty-four male BALB/c mice were randomly divided into three groups: normal control, asthma, AG1478-treated. Mice were sensitized and challenged with ovalbumin (OVA) and a mouse mode1 of asthma was prepared. Collagen deposition was determined in Masson-stained lung sections. Periodic acid Schiff (PAS) staining was used to observe the proliferation of goblet cells. Immunohistochemistry was used to determine the protein expression of HB-EGF. RT-PCR was used to determine the mRNA expression of HB-EGF and EGFR.
RESULTSThe characteristic changes of airway remodeling occurred in the asthma group. The expression of HB-EGF and EGFR in the epithelial cells of bronchi in the asthma group was significantly higher than that in the normal control group. Compared with the asthma group, the AG1478-treated group had decreased inflammation reactions, decreased collagen deposition and proliferation of goblet cells and lower expression of EGFR and HB-EGF.
CONCLUSIONSEGFR tyrosine kinase inhibitor (AG1478) ameliorates the progression of airway remodeling in mice with asthma by inhibitions of EGFR and HB-EGF expression and EGFR signal pathway.