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LncRNA MALAT1 Affects Mycoplasma pneumoniae Pneumonia via NF-κB Regulation
Our aim was to determine whether the long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is involved in Mycoplasma pneumoniae pneumonia (MPP), and its possible mechanism of action. MALAT1 expression in the bronchoalveolar lavage fluid of 50 hospitalized child...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2020
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7561720/ https://www.ncbi.nlm.nih.gov/pubmed/33134293 http://dx.doi.org/10.3389/fcell.2020.563693 |
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author | Gu, Haiyan Zhu, Yifan Zhou, Yao Huang, Tianyu Zhang, Siqing Zhao, Deyu Liu, Feng |
author_facet | Gu, Haiyan Zhu, Yifan Zhou, Yao Huang, Tianyu Zhang, Siqing Zhao, Deyu Liu, Feng |
author_sort | Gu, Haiyan |
collection | PubMed |
description | Our aim was to determine whether the long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is involved in Mycoplasma pneumoniae pneumonia (MPP), and its possible mechanism of action. MALAT1 expression in the bronchoalveolar lavage fluid of 50 hospitalized children with MPP was compared to its expression in 30 children with intrabronchial foreign bodies. MALAT1 expression was higher in children with MPP, accompanied by increased inflammatory mediators interleukin 8 (IL-8) and tumor necrosis factor alpha (TNF-α), compared to the controls. In human airway epithelial cells infected with wild-type Mycoplasma pneumoniae (strain M129), MALAT1, IL-8, and TNF-α expression significantly increased, and increased expression of IL-8 and TNF-α could be suppressed by MALAT1 knockdown. Luciferase reporter gene assay and western blot showed that knockdown of MALAT1 reduced nuclear factor-κB (NF-κB) activation. In vivo, RNAi packaged with adenovirus (Adv) was nasally transfected into BALB/c mice to silence MALAT1, and an MP-infected mouse pneumonia model was prepared. The results demonstrated that the degree of pulmonary inflammatory injury, vascular permeability, secretion of inflammatory factors, and expression of phosphorylated p65 (pp65) in MP-infected mice were partly reversed after MALAT1 knockdown compared to those in the controls. In conclusion, MALAT1 is involved in the regulation of airway and pulmonary inflammation caused by MP infection via NF-κB regulation. |
format | Online Article Text |
id | pubmed-7561720 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-75617202020-10-29 LncRNA MALAT1 Affects Mycoplasma pneumoniae Pneumonia via NF-κB Regulation Gu, Haiyan Zhu, Yifan Zhou, Yao Huang, Tianyu Zhang, Siqing Zhao, Deyu Liu, Feng Front Cell Dev Biol Cell and Developmental Biology Our aim was to determine whether the long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is involved in Mycoplasma pneumoniae pneumonia (MPP), and its possible mechanism of action. MALAT1 expression in the bronchoalveolar lavage fluid of 50 hospitalized children with MPP was compared to its expression in 30 children with intrabronchial foreign bodies. MALAT1 expression was higher in children with MPP, accompanied by increased inflammatory mediators interleukin 8 (IL-8) and tumor necrosis factor alpha (TNF-α), compared to the controls. In human airway epithelial cells infected with wild-type Mycoplasma pneumoniae (strain M129), MALAT1, IL-8, and TNF-α expression significantly increased, and increased expression of IL-8 and TNF-α could be suppressed by MALAT1 knockdown. Luciferase reporter gene assay and western blot showed that knockdown of MALAT1 reduced nuclear factor-κB (NF-κB) activation. In vivo, RNAi packaged with adenovirus (Adv) was nasally transfected into BALB/c mice to silence MALAT1, and an MP-infected mouse pneumonia model was prepared. The results demonstrated that the degree of pulmonary inflammatory injury, vascular permeability, secretion of inflammatory factors, and expression of phosphorylated p65 (pp65) in MP-infected mice were partly reversed after MALAT1 knockdown compared to those in the controls. In conclusion, MALAT1 is involved in the regulation of airway and pulmonary inflammation caused by MP infection via NF-κB regulation. Frontiers Media S.A. 2020-10-02 /pmc/articles/PMC7561720/ /pubmed/33134293 http://dx.doi.org/10.3389/fcell.2020.563693 Text en Copyright © 2020 Gu, Zhu, Zhou, Huang, Zhang, Zhao and Liu. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Cell and Developmental Biology Gu, Haiyan Zhu, Yifan Zhou, Yao Huang, Tianyu Zhang, Siqing Zhao, Deyu Liu, Feng LncRNA MALAT1 Affects Mycoplasma pneumoniae Pneumonia via NF-κB Regulation |
title | LncRNA MALAT1 Affects Mycoplasma pneumoniae Pneumonia via NF-κB Regulation |
title_full | LncRNA MALAT1 Affects Mycoplasma pneumoniae Pneumonia via NF-κB Regulation |
title_fullStr | LncRNA MALAT1 Affects Mycoplasma pneumoniae Pneumonia via NF-κB Regulation |
title_full_unstemmed | LncRNA MALAT1 Affects Mycoplasma pneumoniae Pneumonia via NF-κB Regulation |
title_short | LncRNA MALAT1 Affects Mycoplasma pneumoniae Pneumonia via NF-κB Regulation |
title_sort | lncrna malat1 affects mycoplasma pneumoniae pneumonia via nf-κb regulation |
topic | Cell and Developmental Biology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7561720/ https://www.ncbi.nlm.nih.gov/pubmed/33134293 http://dx.doi.org/10.3389/fcell.2020.563693 |
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