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LncRNA MALAT1 promotes proliferation and migration of airway smooth muscle cells in asthma by downregulating microRNA-216a
Asthma is a difficult chronic airway inflammation, if it cannot be treated and relieved in time, it will seriously affect the health and quality of life of patients. Airway remodeling is relevant to asthma, but there is currently no effective treatment for airway remodeling. Regulating the biologica...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8324955/ https://www.ncbi.nlm.nih.gov/pubmed/34354391 http://dx.doi.org/10.1016/j.sjbs.2021.03.076 |
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author | Huang, Jun Wang, Fang Hun Wang, Long Li, Yong Lu, Junlimeng Chen, JianYou |
author_facet | Huang, Jun Wang, Fang Hun Wang, Long Li, Yong Lu, Junlimeng Chen, JianYou |
author_sort | Huang, Jun |
collection | PubMed |
description | Asthma is a difficult chronic airway inflammation, if it cannot be treated and relieved in time, it will seriously affect the health and quality of life of patients. Airway remodeling is relevant to asthma, but there is currently no effective treatment for airway remodeling. Regulating the biological function of airway smooth muscle cells (AMSCs) may be an important method to inhibit airway remodeling. LncRNA MALAT1 and microRNA-216a are involved in the regulation of AMSCs respectively, but there is no research to prove that they can regulate airway remodeling of asthma through mutual combination. Hence, the aim of the present study was performed to investigate the function of lncRNA MALAT1 and microRNA-216a on AMSCs in asthma. The relationship between lncRNA MALAT1, microRNA-216a and AMSCs was studied by MTT, qPCR, Western blot, Transwell and flow cytometry. The results revealed that lncRNA MALAT1 was up-regulated and microRNA-216a was down-regulated in asthma. lncRNA MALAT1 inhibited microRNA-216a targetedly. Whether downregulating lncRNA MALAT1 or upregulating microRNA-216a, cell proliferation, migration and invasion were reduced and apoptosis increased. Therefore, it is believed that lncRNA MALAT1 promotes proliferation and migration of asthma AMSCs by downregulating microRNA-216a. Since lncRNA MALAT1 and microRNA-216a take part in asthma by jointly regulating the proliferation of airway smooth muscle cells and other biological functions, it would be interesting to study if they become biomarkers of asthma, and relationship between the two in asthma diagnosis and poor prognosis. |
format | Online Article Text |
id | pubmed-8324955 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-83249552021-08-04 LncRNA MALAT1 promotes proliferation and migration of airway smooth muscle cells in asthma by downregulating microRNA-216a Huang, Jun Wang, Fang Hun Wang, Long Li, Yong Lu, Junlimeng Chen, JianYou Saudi J Biol Sci Original Article Asthma is a difficult chronic airway inflammation, if it cannot be treated and relieved in time, it will seriously affect the health and quality of life of patients. Airway remodeling is relevant to asthma, but there is currently no effective treatment for airway remodeling. Regulating the biological function of airway smooth muscle cells (AMSCs) may be an important method to inhibit airway remodeling. LncRNA MALAT1 and microRNA-216a are involved in the regulation of AMSCs respectively, but there is no research to prove that they can regulate airway remodeling of asthma through mutual combination. Hence, the aim of the present study was performed to investigate the function of lncRNA MALAT1 and microRNA-216a on AMSCs in asthma. The relationship between lncRNA MALAT1, microRNA-216a and AMSCs was studied by MTT, qPCR, Western blot, Transwell and flow cytometry. The results revealed that lncRNA MALAT1 was up-regulated and microRNA-216a was down-regulated in asthma. lncRNA MALAT1 inhibited microRNA-216a targetedly. Whether downregulating lncRNA MALAT1 or upregulating microRNA-216a, cell proliferation, migration and invasion were reduced and apoptosis increased. Therefore, it is believed that lncRNA MALAT1 promotes proliferation and migration of asthma AMSCs by downregulating microRNA-216a. Since lncRNA MALAT1 and microRNA-216a take part in asthma by jointly regulating the proliferation of airway smooth muscle cells and other biological functions, it would be interesting to study if they become biomarkers of asthma, and relationship between the two in asthma diagnosis and poor prognosis. Elsevier 2021-08 2021-04-09 /pmc/articles/PMC8324955/ /pubmed/34354391 http://dx.doi.org/10.1016/j.sjbs.2021.03.076 Text en © 2021 Published by Elsevier B.V. on behalf of King Saud University. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Original Article Huang, Jun Wang, Fang Hun Wang, Long Li, Yong Lu, Junlimeng Chen, JianYou LncRNA MALAT1 promotes proliferation and migration of airway smooth muscle cells in asthma by downregulating microRNA-216a |
title | LncRNA MALAT1 promotes proliferation and migration of airway smooth muscle cells in asthma by downregulating microRNA-216a |
title_full | LncRNA MALAT1 promotes proliferation and migration of airway smooth muscle cells in asthma by downregulating microRNA-216a |
title_fullStr | LncRNA MALAT1 promotes proliferation and migration of airway smooth muscle cells in asthma by downregulating microRNA-216a |
title_full_unstemmed | LncRNA MALAT1 promotes proliferation and migration of airway smooth muscle cells in asthma by downregulating microRNA-216a |
title_short | LncRNA MALAT1 promotes proliferation and migration of airway smooth muscle cells in asthma by downregulating microRNA-216a |
title_sort | lncrna malat1 promotes proliferation and migration of airway smooth muscle cells in asthma by downregulating microrna-216a |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8324955/ https://www.ncbi.nlm.nih.gov/pubmed/34354391 http://dx.doi.org/10.1016/j.sjbs.2021.03.076 |
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