MiR-155 contribute to airway inflammation in COPD by regulating autophagy via targeting TLR4/NF-ΚB

Detalhes bibliográficos
Autor(a) principal: WANG,Mingliang
Data de Publicação: 2022
Outros Autores: WANG,Wendong, WANG,Jiashun, ZHANG,Jun
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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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
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