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Dimerized translationally controlled tumor protein increases interleukin-8 expression through MAPK and NF-κB pathways in a human bronchial epithelial cell line

BACKGROUND: Histamine releasing factor (HRF) is a unique cytokine known to regulate a variety of immune cells in late allergic reactions. In the previous study, we revealed that the biologically active form of HRF is the dimerized translationally controlled tumor protein (dTCTP) for the first time,...

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Autores principales: Lee, Heewon, Lee, Kyunglim
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5819651/
https://www.ncbi.nlm.nih.gov/pubmed/29484169
http://dx.doi.org/10.1186/s13578-018-0214-6
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author Lee, Heewon
Lee, Kyunglim
author_facet Lee, Heewon
Lee, Kyunglim
author_sort Lee, Heewon
collection PubMed
description BACKGROUND: Histamine releasing factor (HRF) is a unique cytokine known to regulate a variety of immune cells in late allergic reactions. In the previous study, we revealed that the biologically active form of HRF is the dimerized translationally controlled tumor protein (dTCTP) for the first time, and confirmed the secretion of IL-8 cytokine by dTCTP in human bronchial epithelial cells. However, the signaling pathway by which dTCTP promotes the secretion of IL-8 is not known. RESULTS: When the cells were stimulated with dTCTP, the canonical NF-κB pathway and ERK, JNK and p38 MAPK become activated. dTCTP promoted transcription of IL-8, which involved NF-κB and AP-1 transcription factors. NF-κB was found to be essential for the transcriptional activation of IL-8, while AP-1 was partially responsible for the transcriptional activation by dTCTP. p38 MAPK was found to be involved in post-transcriptional regulation of dTCTP by stabilizing IL-8 mRNA. CONCLUSIONS: This study demonstrated that dTCTP induces IL-8 secretion in BEAS-2B cells through transcriptional and post-transcriptional regulation of MAPK and NF-κB pathways. This study provides insight into the mechanism by which dTCTP induces inflammation. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s13578-018-0214-6) contains supplementary material, which is available to authorized users.
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spelling pubmed-58196512018-02-26 Dimerized translationally controlled tumor protein increases interleukin-8 expression through MAPK and NF-κB pathways in a human bronchial epithelial cell line Lee, Heewon Lee, Kyunglim Cell Biosci Research BACKGROUND: Histamine releasing factor (HRF) is a unique cytokine known to regulate a variety of immune cells in late allergic reactions. In the previous study, we revealed that the biologically active form of HRF is the dimerized translationally controlled tumor protein (dTCTP) for the first time, and confirmed the secretion of IL-8 cytokine by dTCTP in human bronchial epithelial cells. However, the signaling pathway by which dTCTP promotes the secretion of IL-8 is not known. RESULTS: When the cells were stimulated with dTCTP, the canonical NF-κB pathway and ERK, JNK and p38 MAPK become activated. dTCTP promoted transcription of IL-8, which involved NF-κB and AP-1 transcription factors. NF-κB was found to be essential for the transcriptional activation of IL-8, while AP-1 was partially responsible for the transcriptional activation by dTCTP. p38 MAPK was found to be involved in post-transcriptional regulation of dTCTP by stabilizing IL-8 mRNA. CONCLUSIONS: This study demonstrated that dTCTP induces IL-8 secretion in BEAS-2B cells through transcriptional and post-transcriptional regulation of MAPK and NF-κB pathways. This study provides insight into the mechanism by which dTCTP induces inflammation. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s13578-018-0214-6) contains supplementary material, which is available to authorized users. BioMed Central 2018-02-20 /pmc/articles/PMC5819651/ /pubmed/29484169 http://dx.doi.org/10.1186/s13578-018-0214-6 Text en © The Author(s) 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Lee, Heewon
Lee, Kyunglim
Dimerized translationally controlled tumor protein increases interleukin-8 expression through MAPK and NF-κB pathways in a human bronchial epithelial cell line
title Dimerized translationally controlled tumor protein increases interleukin-8 expression through MAPK and NF-κB pathways in a human bronchial epithelial cell line
title_full Dimerized translationally controlled tumor protein increases interleukin-8 expression through MAPK and NF-κB pathways in a human bronchial epithelial cell line
title_fullStr Dimerized translationally controlled tumor protein increases interleukin-8 expression through MAPK and NF-κB pathways in a human bronchial epithelial cell line
title_full_unstemmed Dimerized translationally controlled tumor protein increases interleukin-8 expression through MAPK and NF-κB pathways in a human bronchial epithelial cell line
title_short Dimerized translationally controlled tumor protein increases interleukin-8 expression through MAPK and NF-κB pathways in a human bronchial epithelial cell line
title_sort dimerized translationally controlled tumor protein increases interleukin-8 expression through mapk and nf-κb pathways in a human bronchial epithelial cell line
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5819651/
https://www.ncbi.nlm.nih.gov/pubmed/29484169
http://dx.doi.org/10.1186/s13578-018-0214-6
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AT leekyunglim dimerizedtranslationallycontrolledtumorproteinincreasesinterleukin8expressionthroughmapkandnfkbpathwaysinahumanbronchialepithelialcellline