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Expression of decorin in intestinal tissues of mice with inflammatory bowel disease and its correlation with autophagy

The aim of this study was to investigate the expression of decorin (DCN) in the intestinal tissues of mice with inflammatory bowel disease (IBD) and its correlation with autophagy. The IBD mouse model was created by intrarectal injection of trinitrobenzene sulfonic acid. The pathology of colon tissu...

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Autores principales: Zhao, Huazhou, Xi, Hongqing, Wei, Bo, Cai, Aizhen, Wang, Ting, Wang, Yi, Zhao, Xudong, Song, Yanjing, Chen, Lin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5228524/
https://www.ncbi.nlm.nih.gov/pubmed/28105121
http://dx.doi.org/10.3892/etm.2016.3908
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author Zhao, Huazhou
Xi, Hongqing
Wei, Bo
Cai, Aizhen
Wang, Ting
Wang, Yi
Zhao, Xudong
Song, Yanjing
Chen, Lin
author_facet Zhao, Huazhou
Xi, Hongqing
Wei, Bo
Cai, Aizhen
Wang, Ting
Wang, Yi
Zhao, Xudong
Song, Yanjing
Chen, Lin
author_sort Zhao, Huazhou
collection PubMed
description The aim of this study was to investigate the expression of decorin (DCN) in the intestinal tissues of mice with inflammatory bowel disease (IBD) and its correlation with autophagy. The IBD mouse model was created by intrarectal injection of trinitrobenzene sulfonic acid. The pathology of colon tissues of the mice was examined using hematoxylin and eosin staining. Expression of DCN and the proteins associated with autophagy was detected using immunohistochemistry. Normal human colon mucosal epithelial cells (NCM460 cells) were transfected with DCN expression plasmid and the expression of DCN and autophagy-associated proteins was detected by western blot analysis. Cell apoptosis was studied using an Annexin V apoptosis detection assay and intracellular autophagosomes were observed using electron microscopy. The IBD mouse model was successfully established. Thickening, edema and inflammatory cell infiltration of the intestinal wall were observed in the IBD mice. The expression of DCN as well as the autophagy-associated proteins beclin 1 and LC3B, was increased in the intestinal tissues of the IBD mice. Furthermore, in the NCM460 cells transfected with DCN, the expression of beclin 1 and LC3B was upregulated, while p62 expression was downregulated. Intracellular autophagosomes were increased and apoptosis was decreased in the cells with DCN overexpression. Inhibition of autophagy reversed the effects of DCN on apoptosis. Therefore, DCN is able to induce autophagy and protect intestinal cells during the occurrence and development of IBD.
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spelling pubmed-52285242017-01-19 Expression of decorin in intestinal tissues of mice with inflammatory bowel disease and its correlation with autophagy Zhao, Huazhou Xi, Hongqing Wei, Bo Cai, Aizhen Wang, Ting Wang, Yi Zhao, Xudong Song, Yanjing Chen, Lin Exp Ther Med Articles The aim of this study was to investigate the expression of decorin (DCN) in the intestinal tissues of mice with inflammatory bowel disease (IBD) and its correlation with autophagy. The IBD mouse model was created by intrarectal injection of trinitrobenzene sulfonic acid. The pathology of colon tissues of the mice was examined using hematoxylin and eosin staining. Expression of DCN and the proteins associated with autophagy was detected using immunohistochemistry. Normal human colon mucosal epithelial cells (NCM460 cells) were transfected with DCN expression plasmid and the expression of DCN and autophagy-associated proteins was detected by western blot analysis. Cell apoptosis was studied using an Annexin V apoptosis detection assay and intracellular autophagosomes were observed using electron microscopy. The IBD mouse model was successfully established. Thickening, edema and inflammatory cell infiltration of the intestinal wall were observed in the IBD mice. The expression of DCN as well as the autophagy-associated proteins beclin 1 and LC3B, was increased in the intestinal tissues of the IBD mice. Furthermore, in the NCM460 cells transfected with DCN, the expression of beclin 1 and LC3B was upregulated, while p62 expression was downregulated. Intracellular autophagosomes were increased and apoptosis was decreased in the cells with DCN overexpression. Inhibition of autophagy reversed the effects of DCN on apoptosis. Therefore, DCN is able to induce autophagy and protect intestinal cells during the occurrence and development of IBD. D.A. Spandidos 2016-12 2016-11-15 /pmc/articles/PMC5228524/ /pubmed/28105121 http://dx.doi.org/10.3892/etm.2016.3908 Text en Copyright: © Zhao et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Zhao, Huazhou
Xi, Hongqing
Wei, Bo
Cai, Aizhen
Wang, Ting
Wang, Yi
Zhao, Xudong
Song, Yanjing
Chen, Lin
Expression of decorin in intestinal tissues of mice with inflammatory bowel disease and its correlation with autophagy
title Expression of decorin in intestinal tissues of mice with inflammatory bowel disease and its correlation with autophagy
title_full Expression of decorin in intestinal tissues of mice with inflammatory bowel disease and its correlation with autophagy
title_fullStr Expression of decorin in intestinal tissues of mice with inflammatory bowel disease and its correlation with autophagy
title_full_unstemmed Expression of decorin in intestinal tissues of mice with inflammatory bowel disease and its correlation with autophagy
title_short Expression of decorin in intestinal tissues of mice with inflammatory bowel disease and its correlation with autophagy
title_sort expression of decorin in intestinal tissues of mice with inflammatory bowel disease and its correlation with autophagy
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5228524/
https://www.ncbi.nlm.nih.gov/pubmed/28105121
http://dx.doi.org/10.3892/etm.2016.3908
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