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Blockade of eosinophil-induced bronchial epithelial-mesenchymal transition with a geranyl acetophenone in a coculture model

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-...

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Main Authors: Lee, Yu Zhao, Yap, Hui Min, Shaari, Khozirah, Tham, Chau Ling, Sulaiman, Mohd Roslan, Israf Ali, Daud Ahmad
Format: Article
Language:English
Published: Frontiers Research Foundation 2017
Online Access:http://psasir.upm.edu.my/id/eprint/61018/1/Blockade%20of%20eosinophil-induced%20bronchial%20epithelial-mesenchymal%20transition%20with%20a%20geranyl%20acetophenone%20in%20a%20coculture%20model.pdf
http://psasir.upm.edu.my/id/eprint/61018/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5696322/pdf/fphar-08-00837.pdf
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spelling my.upm.eprints.610182019-04-30T03:45:34Z http://psasir.upm.edu.my/id/eprint/61018/ Blockade of eosinophil-induced bronchial epithelial-mesenchymal transition with a geranyl acetophenone in a coculture model Lee, Yu Zhao Yap, Hui Min Shaari, Khozirah Tham, Chau Ling Sulaiman, Mohd Roslan Israf Ali, Daud Ahmad 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. Frontiers Research Foundation 2017 Article PeerReviewed text en http://psasir.upm.edu.my/id/eprint/61018/1/Blockade%20of%20eosinophil-induced%20bronchial%20epithelial-mesenchymal%20transition%20with%20a%20geranyl%20acetophenone%20in%20a%20coculture%20model.pdf Lee, Yu Zhao and Yap, Hui Min and Shaari, Khozirah and Tham, Chau Ling and Sulaiman, Mohd Roslan and Israf Ali, Daud Ahmad (2017) Blockade of eosinophil-induced bronchial epithelial-mesenchymal transition with a geranyl acetophenone in a coculture model. Frontiers in Pharmacology, 8. pp. 1-13. ISSN ESSN: 1663-9812 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5696322/pdf/fphar-08-00837.pdf 10.3389/fphar.2017.00837
institution Universiti Putra Malaysia
building UPM Library
collection Institutional Repository
continent Asia
country Malaysia
content_provider Universiti Putra Malaysia
content_source UPM Institutional Repository
url_provider http://psasir.upm.edu.my/
language English
description 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.
format Article
author Lee, Yu Zhao
Yap, Hui Min
Shaari, Khozirah
Tham, Chau Ling
Sulaiman, Mohd Roslan
Israf Ali, Daud Ahmad
spellingShingle Lee, Yu Zhao
Yap, Hui Min
Shaari, Khozirah
Tham, Chau Ling
Sulaiman, Mohd Roslan
Israf Ali, Daud Ahmad
Blockade of eosinophil-induced bronchial epithelial-mesenchymal transition with a geranyl acetophenone in a coculture model
author_facet Lee, Yu Zhao
Yap, Hui Min
Shaari, Khozirah
Tham, Chau Ling
Sulaiman, Mohd Roslan
Israf Ali, Daud Ahmad
author_sort Lee, Yu Zhao
title Blockade of eosinophil-induced bronchial epithelial-mesenchymal transition with a geranyl acetophenone in a coculture model
title_short Blockade of eosinophil-induced bronchial epithelial-mesenchymal transition with a geranyl acetophenone in a coculture model
title_full Blockade of eosinophil-induced bronchial epithelial-mesenchymal transition with a geranyl acetophenone in a coculture model
title_fullStr Blockade of eosinophil-induced bronchial epithelial-mesenchymal transition with a geranyl acetophenone in a coculture model
title_full_unstemmed Blockade of eosinophil-induced bronchial epithelial-mesenchymal transition with a geranyl acetophenone in a coculture model
title_sort blockade of eosinophil-induced bronchial epithelial-mesenchymal transition with a geranyl acetophenone in a coculture model
publisher Frontiers Research Foundation
publishDate 2017
url http://psasir.upm.edu.my/id/eprint/61018/1/Blockade%20of%20eosinophil-induced%20bronchial%20epithelial-mesenchymal%20transition%20with%20a%20geranyl%20acetophenone%20in%20a%20coculture%20model.pdf
http://psasir.upm.edu.my/id/eprint/61018/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5696322/pdf/fphar-08-00837.pdf
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score 13.211869

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