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Long noncoding RNA MCM3AP antisense RNA 1 is downregulated in chronic obstructive pulmonary disease and regulates human bronchial smooth muscle cell proliferation
OBJECTIVES: This study aimed to investigate the involvement of MCM3AP antisense RNA 1 (MCM3AP-AS1) in chronic obstructive pulmonary disease (COPD). METHODS: The expression levels of plasma MCM3AP-AS1 in COPD patients and healthy controls were measured by quantitative PCR before treatment and at 3 mo...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
SAGE Publications
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7503009/ https://www.ncbi.nlm.nih.gov/pubmed/32940099 http://dx.doi.org/10.1177/0300060520935215 |
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author | Zhao, Kaishun Tu, Chunlin Liang, Kaiyi Li, Ying Yu, Yanfang |
author_facet | Zhao, Kaishun Tu, Chunlin Liang, Kaiyi Li, Ying Yu, Yanfang |
author_sort | Zhao, Kaishun |
collection | PubMed |
description | OBJECTIVES: This study aimed to investigate the involvement of MCM3AP antisense RNA 1 (MCM3AP-AS1) in chronic obstructive pulmonary disease (COPD). METHODS: The expression levels of plasma MCM3AP-AS1 in COPD patients and healthy controls were measured by quantitative PCR before treatment and at 3 months after the initiation of treatment (post-treatment) from COPD patients. The role of MCM3AP-AS1 in regulating the proliferation of human bronchial smooth muscle cells (HBSMCs) was explored by a cell proliferation assay. RESULTS: We found that MCM3AP-AS1 expression was downregulated in the plasma of COPD patients compared with controls. Among controls, MCM3AP-AS1 expression was lower in smokers than never-smokers. A 3-year follow-up study showed that, among smokers, patients with low MCM3AP-AS1 expression showed a higher incidence of COPD. After treatment for COPD, MCM3AP-AS1 expression significantly increased. The cell proliferation assay showed that MCM3AP-AS1 overexpression decreased the proliferation rate of HBSMCs. MCM3AP-AS1 silencing had the opposite effect. CONCLUSIONS: MCM3AP-AS1 appears to be downregulated in COPD and to predict its occurrence. MCM3AP-AS1 regulates the proliferation of HBSMCs to participate in airway remodeling. |
format | Online Article Text |
id | pubmed-7503009 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-75030092020-09-28 Long noncoding RNA MCM3AP antisense RNA 1 is downregulated in chronic obstructive pulmonary disease and regulates human bronchial smooth muscle cell proliferation Zhao, Kaishun Tu, Chunlin Liang, Kaiyi Li, Ying Yu, Yanfang J Int Med Res Pre-Clinical Research Report OBJECTIVES: This study aimed to investigate the involvement of MCM3AP antisense RNA 1 (MCM3AP-AS1) in chronic obstructive pulmonary disease (COPD). METHODS: The expression levels of plasma MCM3AP-AS1 in COPD patients and healthy controls were measured by quantitative PCR before treatment and at 3 months after the initiation of treatment (post-treatment) from COPD patients. The role of MCM3AP-AS1 in regulating the proliferation of human bronchial smooth muscle cells (HBSMCs) was explored by a cell proliferation assay. RESULTS: We found that MCM3AP-AS1 expression was downregulated in the plasma of COPD patients compared with controls. Among controls, MCM3AP-AS1 expression was lower in smokers than never-smokers. A 3-year follow-up study showed that, among smokers, patients with low MCM3AP-AS1 expression showed a higher incidence of COPD. After treatment for COPD, MCM3AP-AS1 expression significantly increased. The cell proliferation assay showed that MCM3AP-AS1 overexpression decreased the proliferation rate of HBSMCs. MCM3AP-AS1 silencing had the opposite effect. CONCLUSIONS: MCM3AP-AS1 appears to be downregulated in COPD and to predict its occurrence. MCM3AP-AS1 regulates the proliferation of HBSMCs to participate in airway remodeling. SAGE Publications 2020-09-17 /pmc/articles/PMC7503009/ /pubmed/32940099 http://dx.doi.org/10.1177/0300060520935215 Text en © The Author(s) 2020 https://creativecommons.org/licenses/by-nc/4.0/ Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). |
spellingShingle | Pre-Clinical Research Report Zhao, Kaishun Tu, Chunlin Liang, Kaiyi Li, Ying Yu, Yanfang Long noncoding RNA MCM3AP antisense RNA 1 is downregulated in chronic obstructive pulmonary disease and regulates human bronchial smooth muscle cell proliferation |
title | Long noncoding RNA MCM3AP antisense RNA 1 is downregulated in chronic obstructive pulmonary disease and regulates human bronchial smooth muscle cell proliferation |
title_full | Long noncoding RNA MCM3AP antisense RNA 1 is downregulated in chronic obstructive pulmonary disease and regulates human bronchial smooth muscle cell proliferation |
title_fullStr | Long noncoding RNA MCM3AP antisense RNA 1 is downregulated in chronic obstructive pulmonary disease and regulates human bronchial smooth muscle cell proliferation |
title_full_unstemmed | Long noncoding RNA MCM3AP antisense RNA 1 is downregulated in chronic obstructive pulmonary disease and regulates human bronchial smooth muscle cell proliferation |
title_short | Long noncoding RNA MCM3AP antisense RNA 1 is downregulated in chronic obstructive pulmonary disease and regulates human bronchial smooth muscle cell proliferation |
title_sort | long noncoding rna mcm3ap antisense rna 1 is downregulated in chronic obstructive pulmonary disease and regulates human bronchial smooth muscle cell proliferation |
topic | Pre-Clinical Research Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7503009/ https://www.ncbi.nlm.nih.gov/pubmed/32940099 http://dx.doi.org/10.1177/0300060520935215 |
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