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Proteomic identification of moesin upon exposure to acrolein

BACKGROUND: Acrolein (allyl Aldehyde) as one of smoke irritant exacerbates chronic airway diseases and increased in sputum of patients with asthma and chronic obstructive lung disease. But underlying mechanism remains unresolved. The aim of study was to identify protein expression in human lung micr...

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Autores principales: Lee, Pureun-Haneul, Kim, Byeong-Gon, Lee, Sun-Hye, Leikauf, George D., Jang, An-Soo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5773073/
https://www.ncbi.nlm.nih.gov/pubmed/29375273
http://dx.doi.org/10.1186/s12953-017-0130-4
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author Lee, Pureun-Haneul
Kim, Byeong-Gon
Lee, Sun-Hye
Leikauf, George D.
Jang, An-Soo
author_facet Lee, Pureun-Haneul
Kim, Byeong-Gon
Lee, Sun-Hye
Leikauf, George D.
Jang, An-Soo
author_sort Lee, Pureun-Haneul
collection PubMed
description BACKGROUND: Acrolein (allyl Aldehyde) as one of smoke irritant exacerbates chronic airway diseases and increased in sputum of patients with asthma and chronic obstructive lung disease. But underlying mechanism remains unresolved. The aim of study was to identify protein expression in human lung microvascular endothelial cells (HMVEC-L) exposed to acrolein. METHODS: A proteomic approach was used to determine the different expression of proteins at 8 h and 24 h after treatment of acrolein 30 nM and 300 nM to HMVEC-L. Treatment of HMVEC-L with acrolein 30 nM and 300 nM altered 21 protein spots on the two-dimensional gel, and these were then analyzed by MALDI-TOF MS. RESULTS: These proteins included antioxidant, signal transduction, cytoskeleton, protein transduction, catalytic reduction. The proteins were classified into four groups according to the time course of their expression patterns such as continually increasing, transient increasing, transient decreasing, and continually decreasing. For validation immunohistochemical staining and Western blotting was performed on lung tissues from acrolein exposed mice. Moesin was expressed in endothelium, epithelium, and inflammatory cells and increased in lung tissues of acrolein exposed mice compared with sham treated mice. CONCLUSIONS: These results indicate that some of proteins may be an important role for airway disease exacerbation caused by acrolein exposure. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12953-017-0130-4) contains supplementary material, which is available to authorized users.
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spelling pubmed-57730732018-01-26 Proteomic identification of moesin upon exposure to acrolein Lee, Pureun-Haneul Kim, Byeong-Gon Lee, Sun-Hye Leikauf, George D. Jang, An-Soo Proteome Sci Research BACKGROUND: Acrolein (allyl Aldehyde) as one of smoke irritant exacerbates chronic airway diseases and increased in sputum of patients with asthma and chronic obstructive lung disease. But underlying mechanism remains unresolved. The aim of study was to identify protein expression in human lung microvascular endothelial cells (HMVEC-L) exposed to acrolein. METHODS: A proteomic approach was used to determine the different expression of proteins at 8 h and 24 h after treatment of acrolein 30 nM and 300 nM to HMVEC-L. Treatment of HMVEC-L with acrolein 30 nM and 300 nM altered 21 protein spots on the two-dimensional gel, and these were then analyzed by MALDI-TOF MS. RESULTS: These proteins included antioxidant, signal transduction, cytoskeleton, protein transduction, catalytic reduction. The proteins were classified into four groups according to the time course of their expression patterns such as continually increasing, transient increasing, transient decreasing, and continually decreasing. For validation immunohistochemical staining and Western blotting was performed on lung tissues from acrolein exposed mice. Moesin was expressed in endothelium, epithelium, and inflammatory cells and increased in lung tissues of acrolein exposed mice compared with sham treated mice. CONCLUSIONS: These results indicate that some of proteins may be an important role for airway disease exacerbation caused by acrolein exposure. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12953-017-0130-4) contains supplementary material, which is available to authorized users. BioMed Central 2018-01-17 /pmc/articles/PMC5773073/ /pubmed/29375273 http://dx.doi.org/10.1186/s12953-017-0130-4 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, Pureun-Haneul
Kim, Byeong-Gon
Lee, Sun-Hye
Leikauf, George D.
Jang, An-Soo
Proteomic identification of moesin upon exposure to acrolein
title Proteomic identification of moesin upon exposure to acrolein
title_full Proteomic identification of moesin upon exposure to acrolein
title_fullStr Proteomic identification of moesin upon exposure to acrolein
title_full_unstemmed Proteomic identification of moesin upon exposure to acrolein
title_short Proteomic identification of moesin upon exposure to acrolein
title_sort proteomic identification of moesin upon exposure to acrolein
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5773073/
https://www.ncbi.nlm.nih.gov/pubmed/29375273
http://dx.doi.org/10.1186/s12953-017-0130-4
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