MiR-216a reduces apoptosis of pulmonary microvascular endothelial cells in COPD by targeting DNMT1
Introduction Abnormal apoptosis of pulmonary microvascular endothelial cells (PMVECs) participates in the pathogenesis of COPD. Studies have shown that microRNAs (miRNAs) contribute to the pathogenesis of pulmonary diseases by regulating cell apoptosis. The present study aimed to investigate the eff...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
European Publishing
2023-10-01
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| Series: | Tobacco Induced Diseases |
| Subjects: | |
| Online Access: | http://www.tobaccoinduceddiseases.org/MiR-216a-reduces-apoptosis-of-pulmonary-microvascular-nendothelial-cells-in-COPD,171357,0,2.html |
| _version_ | 1797390082115633152 |
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| author | Ling Lin Qing Song Wei Cheng Cong Liu Aiyuan Zhou Zijing Zhou Ping Chen |
| author_facet | Ling Lin Qing Song Wei Cheng Cong Liu Aiyuan Zhou Zijing Zhou Ping Chen |
| author_sort | Ling Lin |
| collection | DOAJ |
| description | Introduction
Abnormal apoptosis of pulmonary microvascular endothelial cells
(PMVECs) participates in the pathogenesis of COPD. Studies have shown that
microRNAs (miRNAs) contribute to the pathogenesis of pulmonary diseases by
regulating cell apoptosis. The present study aimed to investigate the effects of
miR-216a in cigarette smoke extract (CSE)-induced apoptosis of PMVECs in
COPD and explore the potential mechanisms.
Methods
The emphysema model mice were treated with CSE and CS exposure. The
expression of miR-216a and DNA methyltransferase 1 (DNMT1) was assessed in
emphysema mice and COPD patients. The miR-216a mimic and Lenti-DNMT1
were transfected into PMVECs to identify the underlying mechanisms. The
expression levels of miR-216a and DNMT1 were detected by real-time quantitative
polymerase chain reaction (RT-qPCR) or Western blot. Moreover, cell apoptosis
was examined by flow cytometry assays.
Results
The results show that the expression of miR-216a was decreased, whereas
the expression of DNMT1 was increased in the lung tissue of emphysema mice and
COPD patients. In addition, the expression of miR-216a was significantly reduced
in CSE-treated PMVECs, and the overexpression of miR-216a attenuated CSEinduced
PMVEC apoptosis. Furthermore, the expression of DNMT1 was increased
in the CSE-induced PMVECs and then was reduced after the overexpression of
miR-216a in the CSE-stimulated PMVECs. Luciferase reporter assays confirmed
the target reaction between miR-216a and DNMT1. Also, the overexpression of
DNMT1 was able to reverse the anti-apoptotic effect of miR-216a in CSE-induced
PMVECs.
Conclusions
The results indicate that miR-216a may play a crucial role in CSEinduced
apoptosis by directly regulating its target gene DNMT1 in COPD. It
provides insights into the function of MiR-216a/DNMT1 as a potential molecule
in COPD. |
| first_indexed | 2024-03-08T23:06:25Z |
| format | Article |
| id | doaj.art-6f8ef524f0e141bba667ebfa77ad07fd |
| institution | Directory Open Access Journal |
| issn | 1617-9625 |
| language | English |
| last_indexed | 2024-03-08T23:06:25Z |
| publishDate | 2023-10-01 |
| publisher | European Publishing |
| record_format | Article |
| series | Tobacco Induced Diseases |
| spelling | doaj.art-6f8ef524f0e141bba667ebfa77ad07fd2023-12-15T12:41:23ZengEuropean PublishingTobacco Induced Diseases1617-96252023-10-0121October11310.18332/tid/171357171357MiR-216a reduces apoptosis of pulmonary microvascular endothelial cells in COPD by targeting DNMT1Ling Lin0https://orcid.org/0000-0003-4816-1834Qing Song1Wei Cheng2https://orcid.org/0000-0003-1025-0591Cong Liu3Aiyuan Zhou4Zijing Zhou5Ping Chen6https://orcid.org/0000-0001-6707-8636Department of Respiratory and Critical Care Medicine, the Second Xiangya Hospital, Central South University, Changsha, ChinaDepartment of Respiratory and Critical Care Medicine, the Second Xiangya Hospital, Central South University, Changsha, ChinaDepartment of Respiratory and Critical Care Medicine, the Second Xiangya Hospital, Central South University, Changsha, ChinaDepartment of Respiratory and Critical Care Medicine, the Second Xiangya Hospital, Central South University, Changsha, ChinaDepartment of Respiratory and Critical Care Medicine, the Xiangya Hospital, Central South University, Changsha, ChinaDepartment of Respiratory and Critical Care Medicine, the Second Xiangya Hospital, Central South University, Changsha, ChinaDepartment of Respiratory and Critical Care Medicine, the Second Xiangya Hospital, Central South University, Changsha, ChinaIntroduction Abnormal apoptosis of pulmonary microvascular endothelial cells (PMVECs) participates in the pathogenesis of COPD. Studies have shown that microRNAs (miRNAs) contribute to the pathogenesis of pulmonary diseases by regulating cell apoptosis. The present study aimed to investigate the effects of miR-216a in cigarette smoke extract (CSE)-induced apoptosis of PMVECs in COPD and explore the potential mechanisms. Methods The emphysema model mice were treated with CSE and CS exposure. The expression of miR-216a and DNA methyltransferase 1 (DNMT1) was assessed in emphysema mice and COPD patients. The miR-216a mimic and Lenti-DNMT1 were transfected into PMVECs to identify the underlying mechanisms. The expression levels of miR-216a and DNMT1 were detected by real-time quantitative polymerase chain reaction (RT-qPCR) or Western blot. Moreover, cell apoptosis was examined by flow cytometry assays. Results The results show that the expression of miR-216a was decreased, whereas the expression of DNMT1 was increased in the lung tissue of emphysema mice and COPD patients. In addition, the expression of miR-216a was significantly reduced in CSE-treated PMVECs, and the overexpression of miR-216a attenuated CSEinduced PMVEC apoptosis. Furthermore, the expression of DNMT1 was increased in the CSE-induced PMVECs and then was reduced after the overexpression of miR-216a in the CSE-stimulated PMVECs. Luciferase reporter assays confirmed the target reaction between miR-216a and DNMT1. Also, the overexpression of DNMT1 was able to reverse the anti-apoptotic effect of miR-216a in CSE-induced PMVECs. Conclusions The results indicate that miR-216a may play a crucial role in CSEinduced apoptosis by directly regulating its target gene DNMT1 in COPD. It provides insights into the function of MiR-216a/DNMT1 as a potential molecule in COPD.http://www.tobaccoinduceddiseases.org/MiR-216a-reduces-apoptosis-of-pulmonary-microvascular-nendothelial-cells-in-COPD,171357,0,2.htmlchronic obstructive pulmonary diseasemir-216adnmt1pulmonary microvascular endothelial cellsapoptosis |
| spellingShingle | Ling Lin Qing Song Wei Cheng Cong Liu Aiyuan Zhou Zijing Zhou Ping Chen MiR-216a reduces apoptosis of pulmonary microvascular endothelial cells in COPD by targeting DNMT1 Tobacco Induced Diseases chronic obstructive pulmonary disease mir-216a dnmt1 pulmonary microvascular endothelial cells apoptosis |
| title | MiR-216a reduces apoptosis of pulmonary microvascular
endothelial cells in COPD by targeting DNMT1 |
| title_full | MiR-216a reduces apoptosis of pulmonary microvascular
endothelial cells in COPD by targeting DNMT1 |
| title_fullStr | MiR-216a reduces apoptosis of pulmonary microvascular
endothelial cells in COPD by targeting DNMT1 |
| title_full_unstemmed | MiR-216a reduces apoptosis of pulmonary microvascular
endothelial cells in COPD by targeting DNMT1 |
| title_short | MiR-216a reduces apoptosis of pulmonary microvascular
endothelial cells in COPD by targeting DNMT1 |
| title_sort | mir 216a reduces apoptosis of pulmonary microvascular endothelial cells in copd by targeting dnmt1 |
| topic | chronic obstructive pulmonary disease mir-216a dnmt1 pulmonary microvascular endothelial cells apoptosis |
| url | http://www.tobaccoinduceddiseases.org/MiR-216a-reduces-apoptosis-of-pulmonary-microvascular-nendothelial-cells-in-COPD,171357,0,2.html |
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