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MicroRNA-221-3p alleviates cell apoptosis and inflammatory response by targeting cyclin dependent kinase inhibitor 1B in chronic obstructive pulmonary disease

As a chronic bronchitis or emphysema featured by airflow obstruction, chronic obstructive pulmonary disease (COPD) can further develop into respiratory failure and pulmonary heart diseases. MicroRNAs (miRNAs) are crucial mediators in COPD. Nevertheless, the specific role and molecular mechanism of m...

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Autores principales: Yang, Hua, Zhang, Lijuan, Wang, Quandong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8806819/
https://www.ncbi.nlm.nih.gov/pubmed/34516316
http://dx.doi.org/10.1080/21655979.2021.1967837
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author Yang, Hua
Zhang, Lijuan
Wang, Quandong
author_facet Yang, Hua
Zhang, Lijuan
Wang, Quandong
author_sort Yang, Hua
collection PubMed
description As a chronic bronchitis or emphysema featured by airflow obstruction, chronic obstructive pulmonary disease (COPD) can further develop into respiratory failure and pulmonary heart diseases. MicroRNAs (miRNAs) are crucial mediators in COPD. Nevertheless, the specific role and molecular mechanism of microRNA-221-3p (miR-221-3p) in COPD are unclear. This research aimed to probe into the role of miR-221-3p in COPD. Bioinformatics analysis and a series of assays including western blot, luciferase reporter, reverse transcription quantitative polymerase chain reaction, flow cytometry, cell counting kit-8 and enzyme linked immunosorbent assay were used to explore the functions and mechanism of miR-221-3p in COPD. First, miR-221-3p level was validated to be lowly expressed in the lung tissues of COPD patients and 16HBE cells stimulated by cigarette smoke extract (CSE). Functionally, miR-221-3p overexpression inhibited inflammatory response and apoptosis in CSE-treated 16HBE cells. Moreover, we predicted 5 potential targets of miR-221-3p and found that miR-221-3p shared binding site with cyclin dependent kinase inhibitor 1B (CDKN1B). CDKN1B was targeted by miR-221-3p in CSE-treated 16HBE cells. CDKN1B was negatively modulated by miR-221-3p. Finally, rescue experiments demonstrated that overexpressed CDKN1B counteracted the influences of miR-221-3p on apoptosis and inflammatory response in CSE-treated 16HBE cells. Our data showed that miR-221-3p alleviated cell apoptosis and inflammatory response via targeting CDKN1B in an in vitro model of COPD.
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spelling pubmed-88068192022-02-02 MicroRNA-221-3p alleviates cell apoptosis and inflammatory response by targeting cyclin dependent kinase inhibitor 1B in chronic obstructive pulmonary disease Yang, Hua Zhang, Lijuan Wang, Quandong Bioengineered Research Paper As a chronic bronchitis or emphysema featured by airflow obstruction, chronic obstructive pulmonary disease (COPD) can further develop into respiratory failure and pulmonary heart diseases. MicroRNAs (miRNAs) are crucial mediators in COPD. Nevertheless, the specific role and molecular mechanism of microRNA-221-3p (miR-221-3p) in COPD are unclear. This research aimed to probe into the role of miR-221-3p in COPD. Bioinformatics analysis and a series of assays including western blot, luciferase reporter, reverse transcription quantitative polymerase chain reaction, flow cytometry, cell counting kit-8 and enzyme linked immunosorbent assay were used to explore the functions and mechanism of miR-221-3p in COPD. First, miR-221-3p level was validated to be lowly expressed in the lung tissues of COPD patients and 16HBE cells stimulated by cigarette smoke extract (CSE). Functionally, miR-221-3p overexpression inhibited inflammatory response and apoptosis in CSE-treated 16HBE cells. Moreover, we predicted 5 potential targets of miR-221-3p and found that miR-221-3p shared binding site with cyclin dependent kinase inhibitor 1B (CDKN1B). CDKN1B was targeted by miR-221-3p in CSE-treated 16HBE cells. CDKN1B was negatively modulated by miR-221-3p. Finally, rescue experiments demonstrated that overexpressed CDKN1B counteracted the influences of miR-221-3p on apoptosis and inflammatory response in CSE-treated 16HBE cells. Our data showed that miR-221-3p alleviated cell apoptosis and inflammatory response via targeting CDKN1B in an in vitro model of COPD. Taylor & Francis 2021-09-13 /pmc/articles/PMC8806819/ /pubmed/34516316 http://dx.doi.org/10.1080/21655979.2021.1967837 Text en © 2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Paper
Yang, Hua
Zhang, Lijuan
Wang, Quandong
MicroRNA-221-3p alleviates cell apoptosis and inflammatory response by targeting cyclin dependent kinase inhibitor 1B in chronic obstructive pulmonary disease
title MicroRNA-221-3p alleviates cell apoptosis and inflammatory response by targeting cyclin dependent kinase inhibitor 1B in chronic obstructive pulmonary disease
title_full MicroRNA-221-3p alleviates cell apoptosis and inflammatory response by targeting cyclin dependent kinase inhibitor 1B in chronic obstructive pulmonary disease
title_fullStr MicroRNA-221-3p alleviates cell apoptosis and inflammatory response by targeting cyclin dependent kinase inhibitor 1B in chronic obstructive pulmonary disease
title_full_unstemmed MicroRNA-221-3p alleviates cell apoptosis and inflammatory response by targeting cyclin dependent kinase inhibitor 1B in chronic obstructive pulmonary disease
title_short MicroRNA-221-3p alleviates cell apoptosis and inflammatory response by targeting cyclin dependent kinase inhibitor 1B in chronic obstructive pulmonary disease
title_sort microrna-221-3p alleviates cell apoptosis and inflammatory response by targeting cyclin dependent kinase inhibitor 1b in chronic obstructive pulmonary disease
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8806819/
https://www.ncbi.nlm.nih.gov/pubmed/34516316
http://dx.doi.org/10.1080/21655979.2021.1967837
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