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Changes in miRNA Gene Expression during Wound Repair in Differentiated Normal Human Bronchial Epithelium

PURPOSE: Airway epithelium acts as a protective barrier against the particles from the inhaled air. Damage to the epithelium may result in loss of the barrier function. Epithelial repair in response to injury requires complex mechanisms, such as microRNA, small noncoding molecules, to regulate the p...

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Autores principales: Narożna, Beata, Langwiński, Wojciech, Jackson, Claire, Lackie, Peter M., Holloway, John W., Stachowiak, Zuzanna, Dmitrzak-Węglarz, Monika, Szczepankiewicz, Aleksandra
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6145058/
https://www.ncbi.nlm.nih.gov/pubmed/30255030
http://dx.doi.org/10.1155/2018/9093785
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author Narożna, Beata
Langwiński, Wojciech
Jackson, Claire
Lackie, Peter M.
Holloway, John W.
Stachowiak, Zuzanna
Dmitrzak-Węglarz, Monika
Szczepankiewicz, Aleksandra
author_facet Narożna, Beata
Langwiński, Wojciech
Jackson, Claire
Lackie, Peter M.
Holloway, John W.
Stachowiak, Zuzanna
Dmitrzak-Węglarz, Monika
Szczepankiewicz, Aleksandra
author_sort Narożna, Beata
collection PubMed
description PURPOSE: Airway epithelium acts as a protective barrier against the particles from the inhaled air. Damage to the epithelium may result in loss of the barrier function. Epithelial repair in response to injury requires complex mechanisms, such as microRNA, small noncoding molecules, to regulate the processes involved in wound repair. We aimed to establish if the microRNA gene expression profile is altered during the airway epithelial repair in differentiated cells. METHODS: miRNA gene expression profile during the wound closure of differentiated normal human bronchial epithelium (NHBE) from one donor was analysed using quantitative real-time PCR. We have analysed the expression of 754 genes at five time points during a 48-hour period of epithelium repair using TaqMan Low Density Array. RESULTS: We found out that 233 miRNA genes were expressed in normal human bronchial epithelium. Twenty miRNAs were differentially expressed during the wound repair process, but only one (miR-455-3p) showed significance after FDR adjustment (p = 0.02). Using STEM, we have identified two clusters of several miRNA genes with similar expression profile. Pathway enrichment analysis showed several significant signaling pathways altered during repair, mainly involved in cell cycle regulation, proliferation, migration, adhesion, and transcription regulation. CONCLUSIONS: miRNA expression profile is altered during airway epithelial repair of differentiated cells from one donor in response to mechanical injury in vitro, suggesting their potential role in wound repair.
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spelling pubmed-61450582018-09-25 Changes in miRNA Gene Expression during Wound Repair in Differentiated Normal Human Bronchial Epithelium Narożna, Beata Langwiński, Wojciech Jackson, Claire Lackie, Peter M. Holloway, John W. Stachowiak, Zuzanna Dmitrzak-Węglarz, Monika Szczepankiewicz, Aleksandra Int J Genomics Research Article PURPOSE: Airway epithelium acts as a protective barrier against the particles from the inhaled air. Damage to the epithelium may result in loss of the barrier function. Epithelial repair in response to injury requires complex mechanisms, such as microRNA, small noncoding molecules, to regulate the processes involved in wound repair. We aimed to establish if the microRNA gene expression profile is altered during the airway epithelial repair in differentiated cells. METHODS: miRNA gene expression profile during the wound closure of differentiated normal human bronchial epithelium (NHBE) from one donor was analysed using quantitative real-time PCR. We have analysed the expression of 754 genes at five time points during a 48-hour period of epithelium repair using TaqMan Low Density Array. RESULTS: We found out that 233 miRNA genes were expressed in normal human bronchial epithelium. Twenty miRNAs were differentially expressed during the wound repair process, but only one (miR-455-3p) showed significance after FDR adjustment (p = 0.02). Using STEM, we have identified two clusters of several miRNA genes with similar expression profile. Pathway enrichment analysis showed several significant signaling pathways altered during repair, mainly involved in cell cycle regulation, proliferation, migration, adhesion, and transcription regulation. CONCLUSIONS: miRNA expression profile is altered during airway epithelial repair of differentiated cells from one donor in response to mechanical injury in vitro, suggesting their potential role in wound repair. Hindawi 2018-09-05 /pmc/articles/PMC6145058/ /pubmed/30255030 http://dx.doi.org/10.1155/2018/9093785 Text en Copyright © 2018 Beata Narożna et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Narożna, Beata
Langwiński, Wojciech
Jackson, Claire
Lackie, Peter M.
Holloway, John W.
Stachowiak, Zuzanna
Dmitrzak-Węglarz, Monika
Szczepankiewicz, Aleksandra
Changes in miRNA Gene Expression during Wound Repair in Differentiated Normal Human Bronchial Epithelium
title Changes in miRNA Gene Expression during Wound Repair in Differentiated Normal Human Bronchial Epithelium
title_full Changes in miRNA Gene Expression during Wound Repair in Differentiated Normal Human Bronchial Epithelium
title_fullStr Changes in miRNA Gene Expression during Wound Repair in Differentiated Normal Human Bronchial Epithelium
title_full_unstemmed Changes in miRNA Gene Expression during Wound Repair in Differentiated Normal Human Bronchial Epithelium
title_short Changes in miRNA Gene Expression during Wound Repair in Differentiated Normal Human Bronchial Epithelium
title_sort changes in mirna gene expression during wound repair in differentiated normal human bronchial epithelium
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6145058/
https://www.ncbi.nlm.nih.gov/pubmed/30255030
http://dx.doi.org/10.1155/2018/9093785
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