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

Bioengineered

Quandong Wang¹  Hua Yang¹  Lijuan Zhang¹ 

[1] Department of Gerontology, The First People’s Hospital of Lianyungang, Xuzhou Medical University Affiliated Hospital of Lianyungang, Lianyungang, Jiangsu, Chin;

关键词: Mir-221-3p;    CDKN1B;    chronic obstructive pulmonary disease;    6HBE cells;    apoptosis;    inflammatory response;   

DOI  :  10.1080/21655979.2021.1967837

来源: Taylor & Francis

【 摘 要 】

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.

【 授权许可】

CC BY