RRC ID 45083
Author Hosoki K, Kainuma K, Toda M, Harada E, Chelakkot-Govindalayathila AL, Roeen Z, Nagao M, D'Alessandro-Gabazza CN, Fujisawa T, Gabazza EC.
Title Montelukast suppresses epithelial to mesenchymal transition of bronchial epithelial cells induced by eosinophils.
Journal Biochem Biophys Res Commun
Abstract Epithelial to mesenchymal transition (EMT) is a mechanism by which eosinophils can induce airway remodeling. Montelukast, an antagonist of the cysteinyl leukotriene receptor, can suppress airway remodeling in asthma. The purpose of this study was to evaluate whether montelukast can ameliorate airway remodeling by blocking EMT induced by eosinophils. EMT induced was assessed using a co-culture system of human bronchial epithelial cells and human eosinophils or the eosinophilic leukemia cell lines, Eol-1. Montelukast inhibited co-culture associated morphological changes of BEAS-2b cells, decreased the expression of vimentin and collagen I, and increased the expression of E-cadherin. Montelukast mitigated the rise of TGF-β1 production and Smad3 phosphorylation. Co-culture of human eosinophils with BEAS-2B cells significantly enhanced the production of CysLTs compared with BEAS-2B cells or eosinophils alone. The increase of CysLTs was abolished by montelukast pre-treatment. Montelukast had similar effects when co-culture system of Eol-1 and BEAS-2B was used. This study showed that montelukast suppresses eosinophils-induced EMT of airway epithelial cells. This finding may explain the mechanism of montelukast-mediated amelioration of airway remodeling in bronchial asthma.
Volume 449(3)
Pages 351-6
Published 2014-7-4
DOI 10.1016/j.bbrc.2014.05.033
PII S0006-291X(14)00887-0
PMID 24845378
MeSH Acetates / pharmacology* Airway Remodeling / drug effects* Asthma / metabolism Asthma / pathology Bronchi / cytology Bronchi / drug effects* Bronchi / metabolism Cell Line, Tumor Coculture Techniques Collagen Type I / metabolism Cyclopropanes Cysteine / antagonists & inhibitors Eosinophils / physiology Epithelial-Mesenchymal Transition / drug effects* Humans Leukotriene Antagonists / pharmacology* Leukotrienes Phosphorylation Quinolines / pharmacology* Respiratory Mucosa / cytology Respiratory Mucosa / drug effects* Smad3 Protein / metabolism Sulfides Transforming Growth Factor beta1 / metabolism Vimentin / metabolism
IF 2.985
Times Cited 19
WOS Category BIOPHYSICS BIOCHEMISTRY & MOLECULAR BIOLOGY
Resource
Human and Animal Cells EoL-1 cell(RCB0641)