miR-200b regulates cellular senescence and inflammatory responses by targeting ZEB2 in pulmonary emphysema

Smoking is an important factor in the pathogenesis of chronic obstructive pulmonary disease (COPD), which is commonly characterised by cellular senescence and inflammation. Recently, miR-200b has emerged as an important target to cure lung disease; however, the function of miR-200b in reducing cellu...

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Main Authors: Zhiming Shen, Wenting Xuan, Huanhuan Wang, Fei Sun, Chengxin Zhang, Qian Gong, Shenglin Ge
Format: Article
Language:English
Published: Taylor & Francis Group 2020-01-01
Series:Artificial Cells, Nanomedicine, and Biotechnology
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Online Access:https://www.tandfonline.com/doi/10.1080/21691401.2020.1725029
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author Zhiming Shen
Wenting Xuan
Huanhuan Wang
Fei Sun
Chengxin Zhang
Qian Gong
Shenglin Ge
author_facet Zhiming Shen
Wenting Xuan
Huanhuan Wang
Fei Sun
Chengxin Zhang
Qian Gong
Shenglin Ge
author_sort Zhiming Shen
collection DOAJ
description Smoking is an important factor in the pathogenesis of chronic obstructive pulmonary disease (COPD), which is commonly characterised by cellular senescence and inflammation. Recently, miR-200b has emerged as an important target to cure lung disease; however, the function of miR-200b in reducing cellular senescence and inflammatory responses has not been reported. In this study, we found that miR-200b was downregulated in the lungs of COPD model mice, and its expression is correlated with cellular senescence and inflammatory responses. We hypothesised that miR-200b may be a potential novel therapy for treating COPD. We performed senescence-Associated-β-galactosidase (SA-β-GAL) staining, western blot, qRT-PCR and ELISA; our data suggested that miR-200b is an anti-aging factor in the lungs that is involved in inflammatory responses. We also confirmed that ZEB2 (Zinc finger E-box binding homeobox 2) is a target gene of miR-200b using luciferase reporter assay. In addition, we verified the function of ZEB2 in cellular senescence and inflammatory responses through transfection experiments. Moreover, we found that the protective effects of miR-200b are inhibited when cells overexpress the ZEB2 protein. In conclusion, our results suggest that miR-200b may attenuate cellular senescence and inflammatory responses by targeting ZEB2 in pulmonary emphysema.
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series Artificial Cells, Nanomedicine, and Biotechnology
spelling doaj-art-c21cfc20ef334cb2a9e65affe2d8b44f2025-08-20T04:02:41ZengTaylor & Francis GroupArtificial Cells, Nanomedicine, and Biotechnology2169-14012169-141X2020-01-0148165666310.1080/21691401.2020.1725029miR-200b regulates cellular senescence and inflammatory responses by targeting ZEB2 in pulmonary emphysemaZhiming Shen0Wenting Xuan1Huanhuan Wang2Fei Sun3Chengxin Zhang4Qian Gong5Shenglin Ge6Department of Cardiovascular Surgery, First Affiliated Hospital of Anhui Medical University, Hefei, ChinaDepartment of Anesthesiology, Drum Tower Hospital, Medical College of Nanjing University, Nanjing, ChinaDepartment of Radiation Oncology, First Hospital of Jilin University, Changchun, ChinaDepartment of Cardiovascular Surgery, First Affiliated Hospital of Anhui Medical University, Hefei, ChinaDepartment of Cardiovascular Surgery, First Affiliated Hospital of Anhui Medical University, Hefei, ChinaDepartment of Cardiac Intensive Care Unit, First Affiliated Hospital of Anhui Medical University, Hefei, ChinaDepartment of Cardiovascular Surgery, First Affiliated Hospital of Anhui Medical University, Hefei, ChinaSmoking is an important factor in the pathogenesis of chronic obstructive pulmonary disease (COPD), which is commonly characterised by cellular senescence and inflammation. Recently, miR-200b has emerged as an important target to cure lung disease; however, the function of miR-200b in reducing cellular senescence and inflammatory responses has not been reported. In this study, we found that miR-200b was downregulated in the lungs of COPD model mice, and its expression is correlated with cellular senescence and inflammatory responses. We hypothesised that miR-200b may be a potential novel therapy for treating COPD. We performed senescence-Associated-β-galactosidase (SA-β-GAL) staining, western blot, qRT-PCR and ELISA; our data suggested that miR-200b is an anti-aging factor in the lungs that is involved in inflammatory responses. We also confirmed that ZEB2 (Zinc finger E-box binding homeobox 2) is a target gene of miR-200b using luciferase reporter assay. In addition, we verified the function of ZEB2 in cellular senescence and inflammatory responses through transfection experiments. Moreover, we found that the protective effects of miR-200b are inhibited when cells overexpress the ZEB2 protein. In conclusion, our results suggest that miR-200b may attenuate cellular senescence and inflammatory responses by targeting ZEB2 in pulmonary emphysema.https://www.tandfonline.com/doi/10.1080/21691401.2020.1725029miR-200bZEB2pulmonary emphysemacellular senescenceinflammation
spellingShingle Zhiming Shen
Wenting Xuan
Huanhuan Wang
Fei Sun
Chengxin Zhang
Qian Gong
Shenglin Ge
miR-200b regulates cellular senescence and inflammatory responses by targeting ZEB2 in pulmonary emphysema
Artificial Cells, Nanomedicine, and Biotechnology
miR-200b
ZEB2
pulmonary emphysema
cellular senescence
inflammation
title miR-200b regulates cellular senescence and inflammatory responses by targeting ZEB2 in pulmonary emphysema
title_full miR-200b regulates cellular senescence and inflammatory responses by targeting ZEB2 in pulmonary emphysema
title_fullStr miR-200b regulates cellular senescence and inflammatory responses by targeting ZEB2 in pulmonary emphysema
title_full_unstemmed miR-200b regulates cellular senescence and inflammatory responses by targeting ZEB2 in pulmonary emphysema
title_short miR-200b regulates cellular senescence and inflammatory responses by targeting ZEB2 in pulmonary emphysema
title_sort mir 200b regulates cellular senescence and inflammatory responses by targeting zeb2 in pulmonary emphysema
topic miR-200b
ZEB2
pulmonary emphysema
cellular senescence
inflammation
url https://www.tandfonline.com/doi/10.1080/21691401.2020.1725029
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