The effects of the miR-21/SMAD7/TGF-β pathway on Th17 cell differentiation in COPD

Abstract Chronic obstructive pulmonary disease (COPD) is a complex disease with multiple etiologies, while smoking is the most established one. The present study investigated the modulation of T-helper 17 (Th17) cell differentiation by the miR-21/Smad7/TGF-β pathway, and their roles in COPD. Lung ti...

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Autores principales:	Shengyang He, Shenghua Sun, Junjuan Lu, Lili Chen, Xiang Mei, Liqiu Li, Zhengpeng Zeng, Mubin Zhong, Lihua Xie
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/482afa0e19274b279914fab03e5ee907
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spelling	oai:doaj.org-article:482afa0e19274b279914fab03e5ee9072021-12-02T16:31:11ZThe effects of the miR-21/SMAD7/TGF-β pathway on Th17 cell differentiation in COPD10.1038/s41598-021-85637-02045-2322https://doaj.org/article/482afa0e19274b279914fab03e5ee9072021-03-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-85637-0https://doaj.org/toc/2045-2322Abstract Chronic obstructive pulmonary disease (COPD) is a complex disease with multiple etiologies, while smoking is the most established one. The present study investigated the modulation of T-helper 17 (Th17) cell differentiation by the miR-21/Smad7/TGF-β pathway, and their roles in COPD. Lung tissues were obtained from lung cancer patients with or without COPD who underwent lobotomy and the levels of miR-21, TGF-β/Smad signaling molecules, RORγT, and other Th17-related cytokines were detected. Mouse COPD models were built by exposing both wild-type (WT) and miR-21−/− mice to cigarette smoke (CS) and cigarette smoke extract (CSE) intraperitoneal injection. Isolated primary CD4+ T cells were treated with either CS extract, miR-21 mimics or inhibitors, followed by measuring Th17 cells markers and the expression of TGF-β/Smad signaling molecules and RORγT. Increased levels of miR-21, Smad7, phosphorylated (p)-Smad2, p-Smad3, TGF-β, and Th17-related cytokines was detected in the lungs of COPD patients. Lung function in modeled WT mice, but not miR-21−/− ones, deteriorated and the number of inflammatory cells in the lung tissues increased compared to the control WT-mice. Moreover, primary CD4+ lymphocytes tend to differentiate into Th17 cells after the treatment with CSE or miR-21 mimics, and the expression of RORγT and the TGF-β/Smad signaling were all increased, however miR-21 inhibitors worked reversely. Our findings demonstrated that Th17 cells increased under COPD pathogenesis and was partially modulated by the miR-21/Smad7/TGF-β pathway.Shengyang HeShenghua SunJunjuan LuLili ChenXiang MeiLiqiu LiZhengpeng ZengMubin ZhongLihua XieNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-11 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Shengyang He Shenghua Sun Junjuan Lu Lili Chen Xiang Mei Liqiu Li Zhengpeng Zeng Mubin Zhong Lihua Xie The effects of the miR-21/SMAD7/TGF-β pathway on Th17 cell differentiation in COPD
description	Abstract Chronic obstructive pulmonary disease (COPD) is a complex disease with multiple etiologies, while smoking is the most established one. The present study investigated the modulation of T-helper 17 (Th17) cell differentiation by the miR-21/Smad7/TGF-β pathway, and their roles in COPD. Lung tissues were obtained from lung cancer patients with or without COPD who underwent lobotomy and the levels of miR-21, TGF-β/Smad signaling molecules, RORγT, and other Th17-related cytokines were detected. Mouse COPD models were built by exposing both wild-type (WT) and miR-21−/− mice to cigarette smoke (CS) and cigarette smoke extract (CSE) intraperitoneal injection. Isolated primary CD4+ T cells were treated with either CS extract, miR-21 mimics or inhibitors, followed by measuring Th17 cells markers and the expression of TGF-β/Smad signaling molecules and RORγT. Increased levels of miR-21, Smad7, phosphorylated (p)-Smad2, p-Smad3, TGF-β, and Th17-related cytokines was detected in the lungs of COPD patients. Lung function in modeled WT mice, but not miR-21−/− ones, deteriorated and the number of inflammatory cells in the lung tissues increased compared to the control WT-mice. Moreover, primary CD4+ lymphocytes tend to differentiate into Th17 cells after the treatment with CSE or miR-21 mimics, and the expression of RORγT and the TGF-β/Smad signaling were all increased, however miR-21 inhibitors worked reversely. Our findings demonstrated that Th17 cells increased under COPD pathogenesis and was partially modulated by the miR-21/Smad7/TGF-β pathway.
format	article
author	Shengyang He Shenghua Sun Junjuan Lu Lili Chen Xiang Mei Liqiu Li Zhengpeng Zeng Mubin Zhong Lihua Xie
author_facet	Shengyang He Shenghua Sun Junjuan Lu Lili Chen Xiang Mei Liqiu Li Zhengpeng Zeng Mubin Zhong Lihua Xie
author_sort	Shengyang He
title	The effects of the miR-21/SMAD7/TGF-β pathway on Th17 cell differentiation in COPD
title_short	The effects of the miR-21/SMAD7/TGF-β pathway on Th17 cell differentiation in COPD
title_full	The effects of the miR-21/SMAD7/TGF-β pathway on Th17 cell differentiation in COPD
title_fullStr	The effects of the miR-21/SMAD7/TGF-β pathway on Th17 cell differentiation in COPD
title_full_unstemmed	The effects of the miR-21/SMAD7/TGF-β pathway on Th17 cell differentiation in COPD
title_sort	effects of the mir-21/smad7/tgf-β pathway on th17 cell differentiation in copd
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/482afa0e19274b279914fab03e5ee907
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The effects of the miR-21/SMAD7/TGF-β pathway on Th17 cell differentiation in COPD

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