Cargando…

Inhibition of miR-21 ameliorates LPS-induced acute lung injury through increasing B cell lymphoma-2 expression

The aberrant expression of microRNAs (miRNAs) is associated with the pathogenesis of inflammation-related diseases. However, the biological functions of miR-21 in acute lung injury (ALI) remain largely unknown. In this study, the level of miR-21 was obviously increased, but B cell lymphoma-2 (Bcl-2)...

Descripción completa

Detalles Bibliográficos
Autores principales: Ge, Junke, Yao, Yanfen, Jia, Haiyan, Li, Pibao, Sun, Wei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7787552/
https://www.ncbi.nlm.nih.gov/pubmed/32727244
http://dx.doi.org/10.1177/1753425920942574
_version_ 1783632847681093632
author Ge, Junke
Yao, Yanfen
Jia, Haiyan
Li, Pibao
Sun, Wei
author_facet Ge, Junke
Yao, Yanfen
Jia, Haiyan
Li, Pibao
Sun, Wei
author_sort Ge, Junke
collection PubMed
description The aberrant expression of microRNAs (miRNAs) is associated with the pathogenesis of inflammation-related diseases. However, the biological functions of miR-21 in acute lung injury (ALI) remain largely unknown. In this study, the level of miR-21 was obviously increased, but B cell lymphoma-2 (Bcl-2) expression was markedly decreased in LPS-treated human pulmonary alveolar epithelial cells (HPAEpiC). Suppression of miR-21 attenuated LPS-induced apoptosis and inflammation in HPAEpiC and promoted the survival of mice with ALI by decreasing the inflammatory cell count, release of cytokines and permeability in lung tissues. Importantly, Bcl-2 was a direct target of miR-21, and its expression was significantly inhibited by miR-21 mimics at a post-transcriptional level. Besides, Bcl-2 over-expression reversed miR-21-induced apoptosis and inflammation status and showed synergic effects with miR-21 inhibitor in LPS-treated HPAEpiC. In conclusion, inhibition of miR-21 could ameliorate apoptosis and inflammation by restoring the expression of Bcl-2 in LPS-induced HPAEpiC and mice, which might provide therapeutic strategies for the treatment of ALI.
format Online
Article
Text
id pubmed-7787552
institution National Center for Biotechnology Information
language English
publishDate 2020
publisher SAGE Publications
record_format MEDLINE/PubMed
spelling pubmed-77875522021-01-14 Inhibition of miR-21 ameliorates LPS-induced acute lung injury through increasing B cell lymphoma-2 expression Ge, Junke Yao, Yanfen Jia, Haiyan Li, Pibao Sun, Wei Innate Immun Original Articles The aberrant expression of microRNAs (miRNAs) is associated with the pathogenesis of inflammation-related diseases. However, the biological functions of miR-21 in acute lung injury (ALI) remain largely unknown. In this study, the level of miR-21 was obviously increased, but B cell lymphoma-2 (Bcl-2) expression was markedly decreased in LPS-treated human pulmonary alveolar epithelial cells (HPAEpiC). Suppression of miR-21 attenuated LPS-induced apoptosis and inflammation in HPAEpiC and promoted the survival of mice with ALI by decreasing the inflammatory cell count, release of cytokines and permeability in lung tissues. Importantly, Bcl-2 was a direct target of miR-21, and its expression was significantly inhibited by miR-21 mimics at a post-transcriptional level. Besides, Bcl-2 over-expression reversed miR-21-induced apoptosis and inflammation status and showed synergic effects with miR-21 inhibitor in LPS-treated HPAEpiC. In conclusion, inhibition of miR-21 could ameliorate apoptosis and inflammation by restoring the expression of Bcl-2 in LPS-induced HPAEpiC and mice, which might provide therapeutic strategies for the treatment of ALI. SAGE Publications 2020-07-29 2020-11 /pmc/articles/PMC7787552/ /pubmed/32727244 http://dx.doi.org/10.1177/1753425920942574 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 Original Articles
Ge, Junke
Yao, Yanfen
Jia, Haiyan
Li, Pibao
Sun, Wei
Inhibition of miR-21 ameliorates LPS-induced acute lung injury through increasing B cell lymphoma-2 expression
title Inhibition of miR-21 ameliorates LPS-induced acute lung injury through increasing B cell lymphoma-2 expression
title_full Inhibition of miR-21 ameliorates LPS-induced acute lung injury through increasing B cell lymphoma-2 expression
title_fullStr Inhibition of miR-21 ameliorates LPS-induced acute lung injury through increasing B cell lymphoma-2 expression
title_full_unstemmed Inhibition of miR-21 ameliorates LPS-induced acute lung injury through increasing B cell lymphoma-2 expression
title_short Inhibition of miR-21 ameliorates LPS-induced acute lung injury through increasing B cell lymphoma-2 expression
title_sort inhibition of mir-21 ameliorates lps-induced acute lung injury through increasing b cell lymphoma-2 expression
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7787552/
https://www.ncbi.nlm.nih.gov/pubmed/32727244
http://dx.doi.org/10.1177/1753425920942574
work_keys_str_mv AT gejunke inhibitionofmir21ameliorateslpsinducedacutelunginjurythroughincreasingbcelllymphoma2expression
AT yaoyanfen inhibitionofmir21ameliorateslpsinducedacutelunginjurythroughincreasingbcelllymphoma2expression
AT jiahaiyan inhibitionofmir21ameliorateslpsinducedacutelunginjurythroughincreasingbcelllymphoma2expression
AT lipibao inhibitionofmir21ameliorateslpsinducedacutelunginjurythroughincreasingbcelllymphoma2expression
AT sunwei inhibitionofmir21ameliorateslpsinducedacutelunginjurythroughincreasingbcelllymphoma2expression