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RETRACTED ARTICLE: Inhibition of airway inflammation in a cockroach allergen model of asthma by agonists of miRNA-33b
MicroRNAs (miRNAs) play powerful roles in immune function by regulating target genes that mediate cell behavior. It is well known that mast cells have essential effector and immune regulatory functions in IgE-associated allergic disorders and in innate and adaptive immune responses. However, the rol...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5547138/ https://www.ncbi.nlm.nih.gov/pubmed/28785038 http://dx.doi.org/10.1038/s41598-017-07882-6 |
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author | Niu, Ruichao Xiao, Xuping Liu, Bin Li, Yunqiu zhong, Yu Ma, Lijuan |
author_facet | Niu, Ruichao Xiao, Xuping Liu, Bin Li, Yunqiu zhong, Yu Ma, Lijuan |
author_sort | Niu, Ruichao |
collection | PubMed |
description | MicroRNAs (miRNAs) play powerful roles in immune function by regulating target genes that mediate cell behavior. It is well known that mast cells have essential effector and immune regulatory functions in IgE-associated allergic disorders and in innate and adaptive immune responses. However, the role of miRNAs in mediating mast cell functions and the relevant mechanisms require further exploration. The roles of miR-33b in airway inflammation and mast cell functions are still unknown. To examine the role of miR-33b in mouse mast cells in cockroach allergen-induced asthma, we developed a lentiviral system for miRNA-33b overexpression to examine whether miRNA-33b mediates airway inflammation by regulating mast cell function and to evaluate the underlying mechanism. The results showed that miR-33b inhibited cockroach allergen-induced asthma in vivo: in particular, it inhibited T(H)2 cytokine production. In addition, we found that in cells in which miRNA-33b had been transfected, mast cell degranulation was inhibited through suppression of the calcium release and IgE/FcεRI pathway. Our study provides new insight into the roles of miR-33b in asthma and mast cell biology and identifies novel mechanisms that may contribute to mast cell-related pathological conditions in airway inflammation. |
format | Online Article Text |
id | pubmed-5547138 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-55471382017-08-09 RETRACTED ARTICLE: Inhibition of airway inflammation in a cockroach allergen model of asthma by agonists of miRNA-33b Niu, Ruichao Xiao, Xuping Liu, Bin Li, Yunqiu zhong, Yu Ma, Lijuan Sci Rep Article MicroRNAs (miRNAs) play powerful roles in immune function by regulating target genes that mediate cell behavior. It is well known that mast cells have essential effector and immune regulatory functions in IgE-associated allergic disorders and in innate and adaptive immune responses. However, the role of miRNAs in mediating mast cell functions and the relevant mechanisms require further exploration. The roles of miR-33b in airway inflammation and mast cell functions are still unknown. To examine the role of miR-33b in mouse mast cells in cockroach allergen-induced asthma, we developed a lentiviral system for miRNA-33b overexpression to examine whether miRNA-33b mediates airway inflammation by regulating mast cell function and to evaluate the underlying mechanism. The results showed that miR-33b inhibited cockroach allergen-induced asthma in vivo: in particular, it inhibited T(H)2 cytokine production. In addition, we found that in cells in which miRNA-33b had been transfected, mast cell degranulation was inhibited through suppression of the calcium release and IgE/FcεRI pathway. Our study provides new insight into the roles of miR-33b in asthma and mast cell biology and identifies novel mechanisms that may contribute to mast cell-related pathological conditions in airway inflammation. Nature Publishing Group UK 2017-08-07 /pmc/articles/PMC5547138/ /pubmed/28785038 http://dx.doi.org/10.1038/s41598-017-07882-6 Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Niu, Ruichao Xiao, Xuping Liu, Bin Li, Yunqiu zhong, Yu Ma, Lijuan RETRACTED ARTICLE: Inhibition of airway inflammation in a cockroach allergen model of asthma by agonists of miRNA-33b |
title | RETRACTED ARTICLE: Inhibition of airway inflammation in a cockroach allergen model of asthma by agonists of miRNA-33b |
title_full | RETRACTED ARTICLE: Inhibition of airway inflammation in a cockroach allergen model of asthma by agonists of miRNA-33b |
title_fullStr | RETRACTED ARTICLE: Inhibition of airway inflammation in a cockroach allergen model of asthma by agonists of miRNA-33b |
title_full_unstemmed | RETRACTED ARTICLE: Inhibition of airway inflammation in a cockroach allergen model of asthma by agonists of miRNA-33b |
title_short | RETRACTED ARTICLE: Inhibition of airway inflammation in a cockroach allergen model of asthma by agonists of miRNA-33b |
title_sort | retracted article: inhibition of airway inflammation in a cockroach allergen model of asthma by agonists of mirna-33b |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5547138/ https://www.ncbi.nlm.nih.gov/pubmed/28785038 http://dx.doi.org/10.1038/s41598-017-07882-6 |
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