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MicroRNA-322 inhibits inflammatory cytokine expression and promotes cell proliferation in LPS-stimulated murine macrophages by targeting NF-κB1 (p50)

Inflammation is the body’s normal self-protection mechanism to eliminate pathogens and resist pathogen invasion. The excessive inflammatory response may lead to inflammatory lesions. The mechanisms accounting for inflammation remain hazy. miRNAs have been proposed to have crucial effects on inflamma...

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Detalles Bibliográficos
Autores principales: Zhang, Kai, Song, Fengling, Lu, Xiaoxia, Chen, Wenxun, Huang, Chunxiao, Li, Lexing, Liang, Danyang, Cao, Shengbo, Dai, Hanchuan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5240588/
https://www.ncbi.nlm.nih.gov/pubmed/27986864
http://dx.doi.org/10.1042/BSR20160239
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author Zhang, Kai
Song, Fengling
Lu, Xiaoxia
Chen, Wenxun
Huang, Chunxiao
Li, Lexing
Liang, Danyang
Cao, Shengbo
Dai, Hanchuan
author_facet Zhang, Kai
Song, Fengling
Lu, Xiaoxia
Chen, Wenxun
Huang, Chunxiao
Li, Lexing
Liang, Danyang
Cao, Shengbo
Dai, Hanchuan
author_sort Zhang, Kai
collection PubMed
description Inflammation is the body’s normal self-protection mechanism to eliminate pathogens and resist pathogen invasion. The excessive inflammatory response may lead to inflammatory lesions. The mechanisms accounting for inflammation remain hazy. miRNAs have been proposed to have crucial effects on inflammation. In the present study, we reported that lipopolysaccharide (LPS)-stimulation increased the expression levels of inflammatory cytokines and the cell-cycle progression was suppressed in RAW264.7 cells. Meanwhile, the expression of miR-322 was significantly down-regulated after LPS treatment. Bioinformatics predictions revealed a potential binding site of miR-322 in 3′-UTR of NF-κB1 (p50) and it was further confirmed by luciferase assay. Moreover, both the mRNA and protein levels of NF-κB1 (p50) were down-regulated by miR-322 in RAW264.7 cells. Subsequently, we demonstrated that miR-322 mimics decrease in the expression levels of inflammatory cytokines and cell-cycle repression can be rescued following LPS treatment in RAW264.7 cells. The anti-inflammatory cytokines expression including IL-4 and IL-10 were significantly up-regulated. Furthermore, miR-322 could also promote RAW264.7 cells proliferation. These results demonstrate that miR-322 is a negative regulator of inflammatory response by targeting NF-κB1 (p50).
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spelling pubmed-52405882017-02-28 MicroRNA-322 inhibits inflammatory cytokine expression and promotes cell proliferation in LPS-stimulated murine macrophages by targeting NF-κB1 (p50) Zhang, Kai Song, Fengling Lu, Xiaoxia Chen, Wenxun Huang, Chunxiao Li, Lexing Liang, Danyang Cao, Shengbo Dai, Hanchuan Biosci Rep Research Articles Inflammation is the body’s normal self-protection mechanism to eliminate pathogens and resist pathogen invasion. The excessive inflammatory response may lead to inflammatory lesions. The mechanisms accounting for inflammation remain hazy. miRNAs have been proposed to have crucial effects on inflammation. In the present study, we reported that lipopolysaccharide (LPS)-stimulation increased the expression levels of inflammatory cytokines and the cell-cycle progression was suppressed in RAW264.7 cells. Meanwhile, the expression of miR-322 was significantly down-regulated after LPS treatment. Bioinformatics predictions revealed a potential binding site of miR-322 in 3′-UTR of NF-κB1 (p50) and it was further confirmed by luciferase assay. Moreover, both the mRNA and protein levels of NF-κB1 (p50) were down-regulated by miR-322 in RAW264.7 cells. Subsequently, we demonstrated that miR-322 mimics decrease in the expression levels of inflammatory cytokines and cell-cycle repression can be rescued following LPS treatment in RAW264.7 cells. The anti-inflammatory cytokines expression including IL-4 and IL-10 were significantly up-regulated. Furthermore, miR-322 could also promote RAW264.7 cells proliferation. These results demonstrate that miR-322 is a negative regulator of inflammatory response by targeting NF-κB1 (p50). Portland Press Ltd. 2017-01-17 /pmc/articles/PMC5240588/ /pubmed/27986864 http://dx.doi.org/10.1042/BSR20160239 Text en © 2017 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
Zhang, Kai
Song, Fengling
Lu, Xiaoxia
Chen, Wenxun
Huang, Chunxiao
Li, Lexing
Liang, Danyang
Cao, Shengbo
Dai, Hanchuan
MicroRNA-322 inhibits inflammatory cytokine expression and promotes cell proliferation in LPS-stimulated murine macrophages by targeting NF-κB1 (p50)
title MicroRNA-322 inhibits inflammatory cytokine expression and promotes cell proliferation in LPS-stimulated murine macrophages by targeting NF-κB1 (p50)
title_full MicroRNA-322 inhibits inflammatory cytokine expression and promotes cell proliferation in LPS-stimulated murine macrophages by targeting NF-κB1 (p50)
title_fullStr MicroRNA-322 inhibits inflammatory cytokine expression and promotes cell proliferation in LPS-stimulated murine macrophages by targeting NF-κB1 (p50)
title_full_unstemmed MicroRNA-322 inhibits inflammatory cytokine expression and promotes cell proliferation in LPS-stimulated murine macrophages by targeting NF-κB1 (p50)
title_short MicroRNA-322 inhibits inflammatory cytokine expression and promotes cell proliferation in LPS-stimulated murine macrophages by targeting NF-κB1 (p50)
title_sort microrna-322 inhibits inflammatory cytokine expression and promotes cell proliferation in lps-stimulated murine macrophages by targeting nf-κb1 (p50)
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5240588/
https://www.ncbi.nlm.nih.gov/pubmed/27986864
http://dx.doi.org/10.1042/BSR20160239
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