Cargando…
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...
Autores principales: | , , |
---|---|
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 |
_version_ | 1784643547296694272 |
---|---|
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. |
format | Online Article Text |
id | pubmed-8806819 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Taylor & Francis |
record_format | MEDLINE/PubMed |
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 |
work_keys_str_mv | AT yanghua microrna2213palleviatescellapoptosisandinflammatoryresponsebytargetingcyclindependentkinaseinhibitor1binchronicobstructivepulmonarydisease AT zhanglijuan microrna2213palleviatescellapoptosisandinflammatoryresponsebytargetingcyclindependentkinaseinhibitor1binchronicobstructivepulmonarydisease AT wangquandong microrna2213palleviatescellapoptosisandinflammatoryresponsebytargetingcyclindependentkinaseinhibitor1binchronicobstructivepulmonarydisease |