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Profiles of microRNA networks in intestinal epithelial cells in a mouse model of colitis
Inflammatory bowel diseases (IBDs) accompany a critical loss of the frontline barrier function that is achieved primarily by intestinal epithelial cells (IECs). Although the gene-regulation pathways underlying these host-defense roles of IECs presumably are deranged during IBD pathogenesis, the quan...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4673535/ https://www.ncbi.nlm.nih.gov/pubmed/26647826 http://dx.doi.org/10.1038/srep18174 |
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author | Lee, Juneyoung Park, Eun Jeong Yuki, Yoshikazu Ahmad, Shandar Mizuguchi, Kenji Ishii, Ken J. Shimaoka, Motomu Kiyono, Hiroshi |
author_facet | Lee, Juneyoung Park, Eun Jeong Yuki, Yoshikazu Ahmad, Shandar Mizuguchi, Kenji Ishii, Ken J. Shimaoka, Motomu Kiyono, Hiroshi |
author_sort | Lee, Juneyoung |
collection | PubMed |
description | Inflammatory bowel diseases (IBDs) accompany a critical loss of the frontline barrier function that is achieved primarily by intestinal epithelial cells (IECs). Although the gene-regulation pathways underlying these host-defense roles of IECs presumably are deranged during IBD pathogenesis, the quantitative and qualitative alterations of posttranscriptional regulators such as microRNAs (miRNAs) within the cells largely remain to be defined. We aimed to uncover the regulatory miRNA–target gene relationships that arise differentially in inflamed small- compared with large-IECs. Whereas IBD significantly increased the expression of only a few miRNA candidates in small-IECs, numerous miRNAs were upregulated in inflamed large-IECs. These marked alterations might explain why the large, as compared with small, intestine is more sensitive to colitis and shows more severe pathology in this experimental model of IBD. Our in-depth assessment of the miRNA–mRNA expression profiles and the resulting networks prompts us to suggest that miRNAs such as miR-1224, miR-3473a, and miR-5128 represent biomarkers that appear in large-IECs upon IBD development and co-operatively repress the expression of key anti-inflammatory factors. The current study provides insight into gene-regulatory networks in IECs through which dynamic rearrangement of the involved miRNAs modulates the gene expression–regulation machinery between maintaining and disrupting gastrointestinal homeostasis. |
format | Online Article Text |
id | pubmed-4673535 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-46735352015-12-14 Profiles of microRNA networks in intestinal epithelial cells in a mouse model of colitis Lee, Juneyoung Park, Eun Jeong Yuki, Yoshikazu Ahmad, Shandar Mizuguchi, Kenji Ishii, Ken J. Shimaoka, Motomu Kiyono, Hiroshi Sci Rep Article Inflammatory bowel diseases (IBDs) accompany a critical loss of the frontline barrier function that is achieved primarily by intestinal epithelial cells (IECs). Although the gene-regulation pathways underlying these host-defense roles of IECs presumably are deranged during IBD pathogenesis, the quantitative and qualitative alterations of posttranscriptional regulators such as microRNAs (miRNAs) within the cells largely remain to be defined. We aimed to uncover the regulatory miRNA–target gene relationships that arise differentially in inflamed small- compared with large-IECs. Whereas IBD significantly increased the expression of only a few miRNA candidates in small-IECs, numerous miRNAs were upregulated in inflamed large-IECs. These marked alterations might explain why the large, as compared with small, intestine is more sensitive to colitis and shows more severe pathology in this experimental model of IBD. Our in-depth assessment of the miRNA–mRNA expression profiles and the resulting networks prompts us to suggest that miRNAs such as miR-1224, miR-3473a, and miR-5128 represent biomarkers that appear in large-IECs upon IBD development and co-operatively repress the expression of key anti-inflammatory factors. The current study provides insight into gene-regulatory networks in IECs through which dynamic rearrangement of the involved miRNAs modulates the gene expression–regulation machinery between maintaining and disrupting gastrointestinal homeostasis. Nature Publishing Group 2015-12-09 /pmc/articles/PMC4673535/ /pubmed/26647826 http://dx.doi.org/10.1038/srep18174 Text en Copyright © 2015, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Lee, Juneyoung Park, Eun Jeong Yuki, Yoshikazu Ahmad, Shandar Mizuguchi, Kenji Ishii, Ken J. Shimaoka, Motomu Kiyono, Hiroshi Profiles of microRNA networks in intestinal epithelial cells in a mouse model of colitis |
title | Profiles of microRNA networks in intestinal epithelial cells in a mouse model of colitis |
title_full | Profiles of microRNA networks in intestinal epithelial cells in a mouse model of colitis |
title_fullStr | Profiles of microRNA networks in intestinal epithelial cells in a mouse model of colitis |
title_full_unstemmed | Profiles of microRNA networks in intestinal epithelial cells in a mouse model of colitis |
title_short | Profiles of microRNA networks in intestinal epithelial cells in a mouse model of colitis |
title_sort | profiles of microrna networks in intestinal epithelial cells in a mouse model of colitis |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4673535/ https://www.ncbi.nlm.nih.gov/pubmed/26647826 http://dx.doi.org/10.1038/srep18174 |
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