Blockade of Eosinophil-Induced Bronchial Epithelial-Mesenchymal Transition with a Geranyl Acetophenone in a Coculture Model
| Autor: | Chau Ling Tham, Yu Z. Lee, Daud Ahmad Israf, Hui M. Yap, Mohd Roslan Sulaiman, Khozirah Shaari |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
epithelial-mesenchymal transition Vimentin 03 medical and health sciences airway remodeling 0302 clinical medicine geranyl acetophenone medicine Pharmacology (medical) Epithelial–mesenchymal transition Original Research Pharmacology transforming growth factor beta biology lcsh:RM1-950 Transforming growth factor beta Eosinophil respiratory system asthma Cell biology Fibronectin 030104 developmental biology medicine.anatomical_structure lcsh:Therapeutics. Pharmacology Cell culture 030220 oncology & carcinogenesis Immunology biology.protein Signal transduction Transforming growth factor |
| Zdroj: | Frontiers in Pharmacology Frontiers in Pharmacology, Vol 8 (2017) |
| ISSN: | 1663-9812 |
| Popis: | Epithelial-mesenchymal transition (EMT) is currently recognized as the main cellular event that contributes to airway remodeling. Eosinophils can induce EMT in airway epithelial cells via increased transforming growth factor (TGF)-β production. We assessed the effect of synthetic 2,4,6-trihydroxy-3-geranyl acetophenone (tHGA) upon eosinophil-induced EMT in a cellular model. The human eosinophil cell line EoL-1 was used to induce EMT in BEAS-2B human bronchial epithelial cells. The induction of EMT was dose-dependently suppressed following tHGA treatment in which the epithelial morphology and E-cadherin expression were not altered. Protein and mRNA expression of vimentin, collagen I and fibronectin in eosinophil-induced epithelial cells were also significantly suppressed by tHGA treatment. Following pathway analysis, we showed that tHGA suppressed eosinophil-induced activator protein-1-mediated TGF-β production by targeting c-Jun N-terminal kinase and phosphoinositide 3-kinase signaling pathways. These findings corroborated previous findings on the ability of tHGA to inhibit experimental murine airway remodeling. |
| Databáze: | OpenAIRE |
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