Overexpression of MALAT1 Relates to Lung Injury through Sponging miR-425 and Promoting Cell Apoptosis during ARDS

Background. Acute respiratory distress syndrome (ARDS) is a severe form of acute lung injury during which severe inflammatory responses induce cell apoptosis, necrosis, and fibrosis. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a multiple function long noncoding RNA that was fo...

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Main Authors: Lu Wang, Jiao Liu, Wenjie Xie, Guang Li, Lan Yao, Rui Zhang, Bin Xu
Format: Article
Language:English
Published: Wiley 2019-01-01
Series:Canadian Respiratory Journal
Online Access:http://dx.doi.org/10.1155/2019/1871394
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author Lu Wang
Jiao Liu
Wenjie Xie
Guang Li
Lan Yao
Rui Zhang
Bin Xu
author_facet Lu Wang
Jiao Liu
Wenjie Xie
Guang Li
Lan Yao
Rui Zhang
Bin Xu
author_sort Lu Wang
collection DOAJ
description Background. Acute respiratory distress syndrome (ARDS) is a severe form of acute lung injury during which severe inflammatory responses induce cell apoptosis, necrosis, and fibrosis. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a multiple function long noncoding RNA that was found overexpressed during acute lung injury. However, the roles of MALAT1 in ARDS patients are still unknown. Methods. Total RNA was extracted from the plasma, plasma exosome, and peripheral blood mononuclear cells (PBMCs) from 65 ARDS patients and 36 healthy controls. The MALAT1 and six candidate miRNAs levels were detected by qRT-PCR. The interaction between MALAT1 and miR-425 was predicted using a bioinformatics tool and verified by dual luciferase assay. Exosomes from ARDS patients were cultured with A549 and HFL-1 cells to confirm the delivery of miR-425 by exosomes. Cell apoptosis and viability were determined by flow cytometry and MTT assay. Results. We found MALAT1 was significantly increased in the ARDS patients’ plasma and PBMCs. The MALAT1 level in PBMCs was negatively correlated with exosomal miR-425 level. MALAT1 interacted with miR-425 and protected phosphatase and tensin homolog (PTEN) expression in A549 and HFL-1 cells. Exosomes from ARDS patients delivered less miR-425 into A549 and HFL-1 cells and induced cell apoptosis via upregulating PTEN. Conclusion. This study identified increased MALAT1 and decreased miR-425 in ARDS patients and unveiled their roles during the pathogenesis of ARDS.
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spelling doaj-art-067e4cae23c84832ab4608156bfbd12c2025-08-20T03:55:23ZengWileyCanadian Respiratory Journal1198-22411916-72452019-01-01201910.1155/2019/18713941871394Overexpression of MALAT1 Relates to Lung Injury through Sponging miR-425 and Promoting Cell Apoptosis during ARDSLu Wang0Jiao Liu1Wenjie Xie2Guang Li3Lan Yao4Rui Zhang5Bin Xu6Department of Critical Care Medicine, Renmin Hospital of Wuhan University, Wuhan, ChinaDepartment of Critical Care Medicine, School of Medicine, North Ruijin Hospital, Shanghai Jiaotong University, Shanghai, ChinaDepartment of Critical Care Medicine, Renmin Hospital of Wuhan University, Wuhan, ChinaDepartment of Critical Care Medicine, Renmin Hospital of Wuhan University, Wuhan, ChinaDepartment of Critical Care Medicine, Renmin Hospital of Wuhan University, Wuhan, ChinaDepartment of Critical Care Medicine, Renmin Hospital of Wuhan University, Wuhan, ChinaDepartment of Oncology, Renmin Hospital of Wuhan Unversity, Wuhan, ChinaBackground. Acute respiratory distress syndrome (ARDS) is a severe form of acute lung injury during which severe inflammatory responses induce cell apoptosis, necrosis, and fibrosis. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a multiple function long noncoding RNA that was found overexpressed during acute lung injury. However, the roles of MALAT1 in ARDS patients are still unknown. Methods. Total RNA was extracted from the plasma, plasma exosome, and peripheral blood mononuclear cells (PBMCs) from 65 ARDS patients and 36 healthy controls. The MALAT1 and six candidate miRNAs levels were detected by qRT-PCR. The interaction between MALAT1 and miR-425 was predicted using a bioinformatics tool and verified by dual luciferase assay. Exosomes from ARDS patients were cultured with A549 and HFL-1 cells to confirm the delivery of miR-425 by exosomes. Cell apoptosis and viability were determined by flow cytometry and MTT assay. Results. We found MALAT1 was significantly increased in the ARDS patients’ plasma and PBMCs. The MALAT1 level in PBMCs was negatively correlated with exosomal miR-425 level. MALAT1 interacted with miR-425 and protected phosphatase and tensin homolog (PTEN) expression in A549 and HFL-1 cells. Exosomes from ARDS patients delivered less miR-425 into A549 and HFL-1 cells and induced cell apoptosis via upregulating PTEN. Conclusion. This study identified increased MALAT1 and decreased miR-425 in ARDS patients and unveiled their roles during the pathogenesis of ARDS.http://dx.doi.org/10.1155/2019/1871394
spellingShingle Lu Wang
Jiao Liu
Wenjie Xie
Guang Li
Lan Yao
Rui Zhang
Bin Xu
Overexpression of MALAT1 Relates to Lung Injury through Sponging miR-425 and Promoting Cell Apoptosis during ARDS
Canadian Respiratory Journal
title Overexpression of MALAT1 Relates to Lung Injury through Sponging miR-425 and Promoting Cell Apoptosis during ARDS
title_full Overexpression of MALAT1 Relates to Lung Injury through Sponging miR-425 and Promoting Cell Apoptosis during ARDS
title_fullStr Overexpression of MALAT1 Relates to Lung Injury through Sponging miR-425 and Promoting Cell Apoptosis during ARDS
title_full_unstemmed Overexpression of MALAT1 Relates to Lung Injury through Sponging miR-425 and Promoting Cell Apoptosis during ARDS
title_short Overexpression of MALAT1 Relates to Lung Injury through Sponging miR-425 and Promoting Cell Apoptosis during ARDS
title_sort overexpression of malat1 relates to lung injury through sponging mir 425 and promoting cell apoptosis during ards
url http://dx.doi.org/10.1155/2019/1871394
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