C-EBPβ mediates in cigarette/IL-17A-induced bronchial epithelial–mesenchymal transition in COPD mice

Abstract Background Cigarettes smoking and IL-17A contribute to chronic obstructive pulmonary disease (COPD), and have synergistical effect on bronchial epithelial cell proliferation. CCAAT/enhancer-binding protein β (C-EBPβ) could be induced by IL-17A and is up-regulated in COPD. We explored the ef...

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Autores principales:	Shuyuan Chu, Libing Ma, Yashan Wu, Xiaoli Zhao, Bo Xiao, Qilu Pan
Formato:	article
Lenguaje:	EN
Publicado:	BMC 2021
Materias:	Diseases of the respiratory system RC705-779
Acceso en línea:	https://doaj.org/article/0d2a14e3388e4f70bc07cc8c45d92ec4
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spelling	oai:doaj.org-article:0d2a14e3388e4f70bc07cc8c45d92ec42021-11-21T12:39:19ZC-EBPβ mediates in cigarette/IL-17A-induced bronchial epithelial–mesenchymal transition in COPD mice10.1186/s12890-021-01738-61471-2466https://doaj.org/article/0d2a14e3388e4f70bc07cc8c45d92ec42021-11-01T00:00:00Zhttps://doi.org/10.1186/s12890-021-01738-6https://doaj.org/toc/1471-2466Abstract Background Cigarettes smoking and IL-17A contribute to chronic obstructive pulmonary disease (COPD), and have synergistical effect on bronchial epithelial cell proliferation. CCAAT/enhancer-binding protein β (C-EBPβ) could be induced by IL-17A and is up-regulated in COPD. We explored the effect of cigarettes and IL-17 on bronchial epithelial–mesenchymal transition (EMT) in COPD mice and potential mechanism involved with C-EBPβ in this study. Methods COPD model was established with mice by exposing to cigarettes. E-Cadherin, Vimentin, IL-17A and C-EBPβ distributions were detected in lung tissues. Primary bronchial epithelial cells were separated from health mice and cocultured with cigarette smoke extract (CSE) or/and IL-17A. E-Cadherin, Vimentin and IL-17 receptor (IL-17R) expressions in vitro were assessed. When C-EBPβ were silenced by siRNA in cells, E-Cadherin, Vimentin and C-EBPβ expressions were detected. Results E-Cadherin distribution was less and Vimentin distribution was more in bronchus of COPD mice than controls. IL-17A and C-EBPβ expressions were higher in lung tissues of COPD mice than controls. In vitro, C-EBPβ protein expression was highest in CSE + IL-17A group, followed by CSE and IL-17A groups. E-cadherin expression in vitro was lowest and Vimentin expression was highest in CSE + IL-17A group, followed by CSE or IL-17A group. Those could be inhibited by C-EBPβ silenced. Conclusions C-EBPβ mediates in cigarette/IL-17A-induced bronchial EMT in COPD mice. Our findings contribute to a better understanding on the progress from COPD to lung cancers, which will provide novel avenues in preventing tumorigenesis of airway in the context of cigarette smoking.Shuyuan ChuLibing MaYashan WuXiaoli ZhaoBo XiaoQilu PanBMCarticleDiseases of the respiratory systemRC705-779ENBMC Pulmonary Medicine, Vol 21, Iss 1, Pp 1-11 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Diseases of the respiratory system RC705-779
spellingShingle	Diseases of the respiratory system RC705-779 Shuyuan Chu Libing Ma Yashan Wu Xiaoli Zhao Bo Xiao Qilu Pan C-EBPβ mediates in cigarette/IL-17A-induced bronchial epithelial–mesenchymal transition in COPD mice
description	Abstract Background Cigarettes smoking and IL-17A contribute to chronic obstructive pulmonary disease (COPD), and have synergistical effect on bronchial epithelial cell proliferation. CCAAT/enhancer-binding protein β (C-EBPβ) could be induced by IL-17A and is up-regulated in COPD. We explored the effect of cigarettes and IL-17 on bronchial epithelial–mesenchymal transition (EMT) in COPD mice and potential mechanism involved with C-EBPβ in this study. Methods COPD model was established with mice by exposing to cigarettes. E-Cadherin, Vimentin, IL-17A and C-EBPβ distributions were detected in lung tissues. Primary bronchial epithelial cells were separated from health mice and cocultured with cigarette smoke extract (CSE) or/and IL-17A. E-Cadherin, Vimentin and IL-17 receptor (IL-17R) expressions in vitro were assessed. When C-EBPβ were silenced by siRNA in cells, E-Cadherin, Vimentin and C-EBPβ expressions were detected. Results E-Cadherin distribution was less and Vimentin distribution was more in bronchus of COPD mice than controls. IL-17A and C-EBPβ expressions were higher in lung tissues of COPD mice than controls. In vitro, C-EBPβ protein expression was highest in CSE + IL-17A group, followed by CSE and IL-17A groups. E-cadherin expression in vitro was lowest and Vimentin expression was highest in CSE + IL-17A group, followed by CSE or IL-17A group. Those could be inhibited by C-EBPβ silenced. Conclusions C-EBPβ mediates in cigarette/IL-17A-induced bronchial EMT in COPD mice. Our findings contribute to a better understanding on the progress from COPD to lung cancers, which will provide novel avenues in preventing tumorigenesis of airway in the context of cigarette smoking.
format	article
author	Shuyuan Chu Libing Ma Yashan Wu Xiaoli Zhao Bo Xiao Qilu Pan
author_facet	Shuyuan Chu Libing Ma Yashan Wu Xiaoli Zhao Bo Xiao Qilu Pan
author_sort	Shuyuan Chu
title	C-EBPβ mediates in cigarette/IL-17A-induced bronchial epithelial–mesenchymal transition in COPD mice
title_short	C-EBPβ mediates in cigarette/IL-17A-induced bronchial epithelial–mesenchymal transition in COPD mice
title_full	C-EBPβ mediates in cigarette/IL-17A-induced bronchial epithelial–mesenchymal transition in COPD mice
title_fullStr	C-EBPβ mediates in cigarette/IL-17A-induced bronchial epithelial–mesenchymal transition in COPD mice
title_full_unstemmed	C-EBPβ mediates in cigarette/IL-17A-induced bronchial epithelial–mesenchymal transition in COPD mice
title_sort	c-ebpβ mediates in cigarette/il-17a-induced bronchial epithelial–mesenchymal transition in copd mice
publisher	BMC
publishDate	2021
url	https://doaj.org/article/0d2a14e3388e4f70bc07cc8c45d92ec4
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C-EBPβ mediates in cigarette/IL-17A-induced bronchial epithelial–mesenchymal transition in COPD mice

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