miR-146a-5p plays an essential role in the aberrant epithelial-fibroblast cross-talk in COPD.
Osei, ET
Florez-Sampedro, L
Tasena, H
Faiz, A
Noordhoek, JA
Timens, W
Postma, DS
Hackett, TL
Heijink, IH
Brandsma, C-A
- Publisher:
- European Respiratory Society
- Publication Type:
- Journal Article
- Citation:
- European Respiratory Journal, 2017, 49, (5), pp. 1-11
- Issue Date:
- 2017-05
Closed Access
Filename | Description | Size | |||
---|---|---|---|---|---|
1602538.full.pdf | 632.17 kB |
Copyright Clearance Process
- Recently Added
- In Progress
- Closed Access
This item is closed access and not available.
Full metadata record
Field | Value | Language |
---|---|---|
dc.contributor.author | Osei, ET | |
dc.contributor.author | Florez-Sampedro, L | |
dc.contributor.author | Tasena, H | |
dc.contributor.author |
Faiz, A https://orcid.org/0000-0003-1740-3538 |
|
dc.contributor.author | Noordhoek, JA | |
dc.contributor.author | Timens, W | |
dc.contributor.author | Postma, DS | |
dc.contributor.author | Hackett, TL | |
dc.contributor.author | Heijink, IH | |
dc.contributor.author | Brandsma, C-A | |
dc.date.accessioned | 2022-07-08T01:37:55Z | |
dc.date.available | 2017-01-29 | |
dc.date.available | 2022-07-08T01:37:55Z | |
dc.date.issued | 2017-05 | |
dc.identifier.citation | European Respiratory Journal, 2017, 49, (5), pp. 1-11 | |
dc.identifier.issn | 0904-1850 | |
dc.identifier.issn | 1399-3003 | |
dc.identifier.uri | http://hdl.handle.net/10453/158744 | |
dc.description.abstract | We previously reported that epithelial-derived interleukin (IL)-1α drives fibroblast-derived inflammation in the lung epithelial-mesenchymal trophic unit. Since miR-146a-5p has been shown to negatively regulate IL-1 signalling, we investigated the role of miR-146a-5p in the regulation of IL-1α-driven inflammation in chronic obstructive pulmonary disease (COPD).Human bronchial epithelial (16HBE14o-) cells were co-cultured with control and COPD-derived primary human lung fibroblasts (PHLFs), and miR-146a-5p expression was assessed with and without IL-1α neutralising antibody. Genomic DNA was assessed for the presence of the single nucleotide polymorphism (SNP) rs2910164. miR-146a-5p mimics were used for overexpression studies to assess IL-1α-induced signalling and IL-8 production by PHLFs.Co-culture of PHLFs with airway epithelial cells significantly increased the expression of miR-146a-5p and this induction was dependent on epithelial-derived IL-1α. miR-146a-5p overexpression decreased IL-1α-induced IL-8 secretion in PHLFs via downregulation of IL-1 receptor-associated kinase-1. In COPD PHLFs, the induction of miR-146a-5p was significantly less compared with controls and was associated with the SNP rs2910164 (GG allele) in the miR-146a-5p gene.Our results suggest that induction of miR-146a-5p is involved in epithelial-fibroblast communication in the lungs and negatively regulates epithelial-derived IL-1α induction of IL-8 by fibroblasts. The decreased levels of miR-146a-5p in COPD fibroblasts may induce a more pro-inflammatory phenotype, contributing to chronic inflammation in COPD. | |
dc.format | Electronic-Print | |
dc.language | eng | |
dc.publisher | European Respiratory Society | |
dc.relation.ispartof | European Respiratory Journal | |
dc.relation.isbasedon | 10.1183/13993003.02538-2016 | |
dc.rights | info:eu-repo/semantics/closedAccess | |
dc.subject.classification | Respiratory System | |
dc.subject.mesh | Alleles | |
dc.subject.mesh | Antibodies, Neutralizing | |
dc.subject.mesh | Bronchi | |
dc.subject.mesh | Cell Line, Tumor | |
dc.subject.mesh | Cigarette Smoking | |
dc.subject.mesh | Coculture Techniques | |
dc.subject.mesh | Culture Media, Conditioned | |
dc.subject.mesh | Epithelial Cells | |
dc.subject.mesh | Epithelium | |
dc.subject.mesh | Fibroblasts | |
dc.subject.mesh | Humans | |
dc.subject.mesh | Inflammation | |
dc.subject.mesh | Interleukin-1alpha | |
dc.subject.mesh | Interleukin-8 | |
dc.subject.mesh | MicroRNAs | |
dc.subject.mesh | Polymorphism, Single Nucleotide | |
dc.subject.mesh | Pulmonary Disease, Chronic Obstructive | |
dc.subject.mesh | Signal Transduction | |
dc.subject.mesh | Tobacco Products | |
dc.subject.mesh | Alleles | |
dc.subject.mesh | Antibodies, Neutralizing | |
dc.subject.mesh | Bronchi | |
dc.subject.mesh | Cell Line, Tumor | |
dc.subject.mesh | Cigarette Smoking | |
dc.subject.mesh | Coculture Techniques | |
dc.subject.mesh | Culture Media, Conditioned | |
dc.subject.mesh | Epithelial Cells | |
dc.subject.mesh | Epithelium | |
dc.subject.mesh | Fibroblasts | |
dc.subject.mesh | Humans | |
dc.subject.mesh | Inflammation | |
dc.subject.mesh | Interleukin-1alpha | |
dc.subject.mesh | Interleukin-8 | |
dc.subject.mesh | MicroRNAs | |
dc.subject.mesh | Polymorphism, Single Nucleotide | |
dc.subject.mesh | Pulmonary Disease, Chronic Obstructive | |
dc.subject.mesh | Signal Transduction | |
dc.subject.mesh | Tobacco Products | |
dc.subject.mesh | Bronchi | |
dc.subject.mesh | Epithelium | |
dc.subject.mesh | Cell Line, Tumor | |
dc.subject.mesh | Fibroblasts | |
dc.subject.mesh | Epithelial Cells | |
dc.subject.mesh | Humans | |
dc.subject.mesh | Pulmonary Disease, Chronic Obstructive | |
dc.subject.mesh | Inflammation | |
dc.subject.mesh | MicroRNAs | |
dc.subject.mesh | Interleukin-8 | |
dc.subject.mesh | Culture Media, Conditioned | |
dc.subject.mesh | Coculture Techniques | |
dc.subject.mesh | Signal Transduction | |
dc.subject.mesh | Polymorphism, Single Nucleotide | |
dc.subject.mesh | Alleles | |
dc.subject.mesh | Interleukin-1alpha | |
dc.subject.mesh | Antibodies, Neutralizing | |
dc.subject.mesh | Tobacco Products | |
dc.subject.mesh | Cigarette Smoking | |
dc.title | miR-146a-5p plays an essential role in the aberrant epithelial-fibroblast cross-talk in COPD. | |
dc.type | Journal Article | |
utslib.citation.volume | 49 | |
utslib.location.activity | England | |
pubs.organisational-group | /University of Technology Sydney | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science/School of Life Sciences | |
pubs.organisational-group | /University of Technology Sydney/Centre for Health Technologies (CHT) | |
utslib.copyright.status | closed_access | * |
pubs.consider-herdc | false | |
dc.date.updated | 2022-07-08T01:37:54Z | |
pubs.issue | 5 | |
pubs.publication-status | Published | |
pubs.volume | 49 | |
utslib.citation.issue | 5 |
Abstract:
We previously reported that epithelial-derived interleukin (IL)-1α drives fibroblast-derived inflammation in the lung epithelial-mesenchymal trophic unit. Since miR-146a-5p has been shown to negatively regulate IL-1 signalling, we investigated the role of miR-146a-5p in the regulation of IL-1α-driven inflammation in chronic obstructive pulmonary disease (COPD).Human bronchial epithelial (16HBE14o-) cells were co-cultured with control and COPD-derived primary human lung fibroblasts (PHLFs), and miR-146a-5p expression was assessed with and without IL-1α neutralising antibody. Genomic DNA was assessed for the presence of the single nucleotide polymorphism (SNP) rs2910164. miR-146a-5p mimics were used for overexpression studies to assess IL-1α-induced signalling and IL-8 production by PHLFs.Co-culture of PHLFs with airway epithelial cells significantly increased the expression of miR-146a-5p and this induction was dependent on epithelial-derived IL-1α. miR-146a-5p overexpression decreased IL-1α-induced IL-8 secretion in PHLFs via downregulation of IL-1 receptor-associated kinase-1. In COPD PHLFs, the induction of miR-146a-5p was significantly less compared with controls and was associated with the SNP rs2910164 (GG allele) in the miR-146a-5p gene.Our results suggest that induction of miR-146a-5p is involved in epithelial-fibroblast communication in the lungs and negatively regulates epithelial-derived IL-1α induction of IL-8 by fibroblasts. The decreased levels of miR-146a-5p in COPD fibroblasts may induce a more pro-inflammatory phenotype, contributing to chronic inflammation in COPD.
Please use this identifier to cite or link to this item:
Download statistics for the last 12 months
Not enough data to produce graph