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MiR-302e attenuates allergic inflammation in vitro model by targeting RelA

Allergic inflammation is the foundation of allergic rhinitis and asthma. Although microRNAs are implicated in the pathogenesis of various diseases, information regarding the functional role of microRNAs in allergic diseases is limited. Herein, we reported that microRNA-302e (miR-302e) serves as an i...

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Detalles Bibliográficos
Autores principales: Xiao, Lifeng, Jiang, Li, Hu, Qi, Li, Yuru
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6435536/
https://www.ncbi.nlm.nih.gov/pubmed/29748238
http://dx.doi.org/10.1042/BSR20180025
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author Xiao, Lifeng
Jiang, Li
Hu, Qi
Li, Yuru
author_facet Xiao, Lifeng
Jiang, Li
Hu, Qi
Li, Yuru
author_sort Xiao, Lifeng
collection PubMed
description Allergic inflammation is the foundation of allergic rhinitis and asthma. Although microRNAs are implicated in the pathogenesis of various diseases, information regarding the functional role of microRNAs in allergic diseases is limited. Herein, we reported that microRNA-302e (miR-302e) serves as an important regulator of allergic inflammation in human mast cell line, HMC-1 cells. Our results showed that miR-302e is the dominant member of miR-302 family expressed in HMC-1 cells. Moreover, the expression of miR-302e was significantly decreased in response to phorbol 12-myristate 13-acetate (PMA) and calcium ionophore A23187 or ovalbumin (OVA) stimulation. Overexpression of miR-302e blocked PMA/A23187 or OVA induced the increase in inflammatory cytokines levels, such as IL-1β, IL-6, tumor necrosis factor (TNF)-α and thymic stromal lymphopoietin, while miR-302 inhibition further promoted the release of these cytokines. Mechanistically, we found that miR-302e is a novel miRNA that targets RelA, a gene known to be involved in regulating inflammation, through binding to the 3′-UTR of RelA mRNA. Ectopic miR-302e remarkably suppressed the luciferase activity and expression of RelA, whereas down-regulation of miR-302e increased RelA luciferase activity and expression. Pharmacological inhibition of NF-κB reversed the augmented effect of miR-302e down-regulation on inflammatory cytokines level. Taken together, the present study demonstrates miR-302e limits allergic inflammation through inhibition of NF-κB activation, suggesting miR-302e may play an anti-inflammatory role in allergic diseases and function as a novel therapeutic target for the treatment of these diseases.
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spelling pubmed-64355362019-04-12 MiR-302e attenuates allergic inflammation in vitro model by targeting RelA Xiao, Lifeng Jiang, Li Hu, Qi Li, Yuru Biosci Rep Research Articles Allergic inflammation is the foundation of allergic rhinitis and asthma. Although microRNAs are implicated in the pathogenesis of various diseases, information regarding the functional role of microRNAs in allergic diseases is limited. Herein, we reported that microRNA-302e (miR-302e) serves as an important regulator of allergic inflammation in human mast cell line, HMC-1 cells. Our results showed that miR-302e is the dominant member of miR-302 family expressed in HMC-1 cells. Moreover, the expression of miR-302e was significantly decreased in response to phorbol 12-myristate 13-acetate (PMA) and calcium ionophore A23187 or ovalbumin (OVA) stimulation. Overexpression of miR-302e blocked PMA/A23187 or OVA induced the increase in inflammatory cytokines levels, such as IL-1β, IL-6, tumor necrosis factor (TNF)-α and thymic stromal lymphopoietin, while miR-302 inhibition further promoted the release of these cytokines. Mechanistically, we found that miR-302e is a novel miRNA that targets RelA, a gene known to be involved in regulating inflammation, through binding to the 3′-UTR of RelA mRNA. Ectopic miR-302e remarkably suppressed the luciferase activity and expression of RelA, whereas down-regulation of miR-302e increased RelA luciferase activity and expression. Pharmacological inhibition of NF-κB reversed the augmented effect of miR-302e down-regulation on inflammatory cytokines level. Taken together, the present study demonstrates miR-302e limits allergic inflammation through inhibition of NF-κB activation, suggesting miR-302e may play an anti-inflammatory role in allergic diseases and function as a novel therapeutic target for the treatment of these diseases. Portland Press Ltd. 2018-05-28 /pmc/articles/PMC6435536/ /pubmed/29748238 http://dx.doi.org/10.1042/BSR20180025 Text en © 2018 The Author(s). http://creativecommons.org/licenses/by/4.0/This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY) (http://creativecommons.org/licenses/by/4.0/) .
spellingShingle Research Articles
Xiao, Lifeng
Jiang, Li
Hu, Qi
Li, Yuru
MiR-302e attenuates allergic inflammation in vitro model by targeting RelA
title MiR-302e attenuates allergic inflammation in vitro model by targeting RelA
title_full MiR-302e attenuates allergic inflammation in vitro model by targeting RelA
title_fullStr MiR-302e attenuates allergic inflammation in vitro model by targeting RelA
title_full_unstemmed MiR-302e attenuates allergic inflammation in vitro model by targeting RelA
title_short MiR-302e attenuates allergic inflammation in vitro model by targeting RelA
title_sort mir-302e attenuates allergic inflammation in vitro model by targeting rela
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6435536/
https://www.ncbi.nlm.nih.gov/pubmed/29748238
http://dx.doi.org/10.1042/BSR20180025
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