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Synergistic action of endothelin (ET)‐1 on the activation of bronchial fibroblast isolated from normal and asthmatic subjects
Author(s) -
Dubé Jean,
Chakir Jamila,
Dubé Carl,
Grimard Yan,
Laviolette Michel,
Boulet LouisPhilippe
Publication year - 2000
Publication title -
international journal of experimental pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.671
H-Index - 72
eISSN - 1365-2613
pISSN - 0959-9673
DOI - 10.1046/j.1365-2613.2000.00173.x
Subject(s) - fibroblast , platelet derived growth factor receptor , platelet derived growth factor , extracellular matrix , fibrosis , submucosa , growth factor , transforming growth factor , endothelin 1 , medicine , immunology , chemistry , endocrinology , in vitro , biochemistry , receptor
Bronchial subepithelial fibrosis is an histological characteristic of asthma. Cytokines and other mediators, such as PDGF‐BB, TGF‐β1 and ET‐1 found in the asthmatic submucosa can potentially activate a repair process that leads to fibroblast proliferation and collagen synthesis. The mechanisms of modulation of the repair process leading to extracellular matrix deposition are still to be documented. In this study, we assessed the in vitro proliferation and collagen synthesis of bronchial fibroblasts isolated from normal and asthmatic subjects in response to ET‐1, platelet‐derived growth factor (PDGF)‐BB and transforming growth factor (TGF)‐β1 alone or in combination, in the presence or absence of dexamethasone. The combination of ET‐1 with one of the other two growth factors, or the triple combination, significantly increased DNA synthesis and collagen production of bronchial fibroblasts isolated from both normal and asthmatic subjects, but the same growth factors used separately had no significant effect on the same parameters. These results suggest that the simultaneous presence of ET‐1, PDGF‐BB and TGF‐β1 in both normal and asthmatic subjects is necessary to activate bronchial fibroblast proliferation and collagen synthesis. As these mediators are present in the submucosa of the asthmatic bronchi, they could be responsible, at least in part, for the accumulation of collagen in the mucosa.