MiR-155 contribute to airway inflammation in COPD by regulating autophagy via targeting TLR4/NF-ΚB
Autor(a) principal: | |
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Data de Publicação: | 2022 |
Outros Autores: | , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Food Science and Technology (Campinas) |
Texto Completo: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-20612022000100662 |
Resumo: | Abstract To evaluate the expression of miR-155 and autophagy in COPD and the related mechanism. Alveolar macrophages were extracted from COPD patients. COPD dynamic mouse model was established. Mouse alveolar macrophages were also isolated and cultured. Rat alveolar macrophage cell line NR8383 was introduced. The expression of TLR4 and NF-κB in NR8383 cells with CSE treatment was also evaluated. miR-155 was upregulated in alveolar macrophages from bronchoalveolar lavage fluid of COPD patients, COPD dynamic mouse model and CSE treated NR8383 cell line (p < 0.05). Overexpression of miR‐155 led to dysregulation of cell autophagy and was closely. miR‐155 promoted cell autophagy by directly targeting TLR4/NF-κB pathway in NR8383 cell line. Our study revealed a novel inflammatory role of miR-155 in COPD and the related mechanisms. We provide a new perspective to understand the pathogenesis of COPD, and miR-155 might be useful as potential target for the treatment of COPD. |
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Food Science and Technology (Campinas) |
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spelling |
MiR-155 contribute to airway inflammation in COPD by regulating autophagy via targeting TLR4/NF-ΚBautophagymiR-155airway inflammationCOPDAbstract To evaluate the expression of miR-155 and autophagy in COPD and the related mechanism. Alveolar macrophages were extracted from COPD patients. COPD dynamic mouse model was established. Mouse alveolar macrophages were also isolated and cultured. Rat alveolar macrophage cell line NR8383 was introduced. The expression of TLR4 and NF-κB in NR8383 cells with CSE treatment was also evaluated. miR-155 was upregulated in alveolar macrophages from bronchoalveolar lavage fluid of COPD patients, COPD dynamic mouse model and CSE treated NR8383 cell line (p < 0.05). Overexpression of miR‐155 led to dysregulation of cell autophagy and was closely. miR‐155 promoted cell autophagy by directly targeting TLR4/NF-κB pathway in NR8383 cell line. Our study revealed a novel inflammatory role of miR-155 in COPD and the related mechanisms. We provide a new perspective to understand the pathogenesis of COPD, and miR-155 might be useful as potential target for the treatment of COPD.Sociedade Brasileira de Ciência e Tecnologia de Alimentos2022-01-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-20612022000100662Food Science and Technology v.42 2022reponame:Food Science and Technology (Campinas)instname:Sociedade Brasileira de Ciência e Tecnologia de Alimentos (SBCTA)instacron:SBCTA10.1590/fst.44321info:eu-repo/semantics/openAccessWANG,MingliangWANG,WendongWANG,JiashunZHANG,Juneng2022-02-23T00:00:00Zoai:scielo:S0101-20612022000100662Revistahttp://www.scielo.br/ctaONGhttps://old.scielo.br/oai/scielo-oai.php||revista@sbcta.org.br1678-457X0101-2061opendoar:2022-02-23T00:00Food Science and Technology (Campinas) - Sociedade Brasileira de Ciência e Tecnologia de Alimentos (SBCTA)false |
dc.title.none.fl_str_mv |
MiR-155 contribute to airway inflammation in COPD by regulating autophagy via targeting TLR4/NF-ΚB |
title |
MiR-155 contribute to airway inflammation in COPD by regulating autophagy via targeting TLR4/NF-ΚB |
spellingShingle |
MiR-155 contribute to airway inflammation in COPD by regulating autophagy via targeting TLR4/NF-ΚB WANG,Mingliang autophagy miR-155 airway inflammation COPD |
title_short |
MiR-155 contribute to airway inflammation in COPD by regulating autophagy via targeting TLR4/NF-ΚB |
title_full |
MiR-155 contribute to airway inflammation in COPD by regulating autophagy via targeting TLR4/NF-ΚB |
title_fullStr |
MiR-155 contribute to airway inflammation in COPD by regulating autophagy via targeting TLR4/NF-ΚB |
title_full_unstemmed |
MiR-155 contribute to airway inflammation in COPD by regulating autophagy via targeting TLR4/NF-ΚB |
title_sort |
MiR-155 contribute to airway inflammation in COPD by regulating autophagy via targeting TLR4/NF-ΚB |
author |
WANG,Mingliang |
author_facet |
WANG,Mingliang WANG,Wendong WANG,Jiashun ZHANG,Jun |
author_role |
author |
author2 |
WANG,Wendong WANG,Jiashun ZHANG,Jun |
author2_role |
author author author |
dc.contributor.author.fl_str_mv |
WANG,Mingliang WANG,Wendong WANG,Jiashun ZHANG,Jun |
dc.subject.por.fl_str_mv |
autophagy miR-155 airway inflammation COPD |
topic |
autophagy miR-155 airway inflammation COPD |
description |
Abstract To evaluate the expression of miR-155 and autophagy in COPD and the related mechanism. Alveolar macrophages were extracted from COPD patients. COPD dynamic mouse model was established. Mouse alveolar macrophages were also isolated and cultured. Rat alveolar macrophage cell line NR8383 was introduced. The expression of TLR4 and NF-κB in NR8383 cells with CSE treatment was also evaluated. miR-155 was upregulated in alveolar macrophages from bronchoalveolar lavage fluid of COPD patients, COPD dynamic mouse model and CSE treated NR8383 cell line (p < 0.05). Overexpression of miR‐155 led to dysregulation of cell autophagy and was closely. miR‐155 promoted cell autophagy by directly targeting TLR4/NF-κB pathway in NR8383 cell line. Our study revealed a novel inflammatory role of miR-155 in COPD and the related mechanisms. We provide a new perspective to understand the pathogenesis of COPD, and miR-155 might be useful as potential target for the treatment of COPD. |
publishDate |
2022 |
dc.date.none.fl_str_mv |
2022-01-01 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-20612022000100662 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-20612022000100662 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.1590/fst.44321 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
text/html |
dc.publisher.none.fl_str_mv |
Sociedade Brasileira de Ciência e Tecnologia de Alimentos |
publisher.none.fl_str_mv |
Sociedade Brasileira de Ciência e Tecnologia de Alimentos |
dc.source.none.fl_str_mv |
Food Science and Technology v.42 2022 reponame:Food Science and Technology (Campinas) instname:Sociedade Brasileira de Ciência e Tecnologia de Alimentos (SBCTA) instacron:SBCTA |
instname_str |
Sociedade Brasileira de Ciência e Tecnologia de Alimentos (SBCTA) |
instacron_str |
SBCTA |
institution |
SBCTA |
reponame_str |
Food Science and Technology (Campinas) |
collection |
Food Science and Technology (Campinas) |
repository.name.fl_str_mv |
Food Science and Technology (Campinas) - Sociedade Brasileira de Ciência e Tecnologia de Alimentos (SBCTA) |
repository.mail.fl_str_mv |
||revista@sbcta.org.br |
_version_ |
1752126332429402112 |