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Intestinal epithelial cells related lncRNA and mRNA expression profiles in dextran sulphate sodium‐induced colitis

Intestinal epithelial barrier damage caused by intestinal epithelial cells (IECs) dysfunction plays a crucial role in the pathogenesis and development of inflammatory bowel disease (IBD). Recently, some studies have suggested the emerging role of long non‐coding RNAs (lncRNAs) in IBD. The aim of thi...

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Autores principales: Liu, Huan, Li, Teming, Zhong, Shizhen, Yu, Min, Huang, Wenhua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7812259/
https://www.ncbi.nlm.nih.gov/pubmed/33300279
http://dx.doi.org/10.1111/jcmm.16174
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author Liu, Huan
Li, Teming
Zhong, Shizhen
Yu, Min
Huang, Wenhua
author_facet Liu, Huan
Li, Teming
Zhong, Shizhen
Yu, Min
Huang, Wenhua
author_sort Liu, Huan
collection PubMed
description Intestinal epithelial barrier damage caused by intestinal epithelial cells (IECs) dysfunction plays a crucial role in the pathogenesis and development of inflammatory bowel disease (IBD). Recently, some studies have suggested the emerging role of long non‐coding RNAs (lncRNAs) in IBD. The aim of this study was to reveal lncRNAs and mRNA expression profiles in IECs from a mouse model of colitis and to expand our understanding in the intestinal epithelial barrier regulation. IECs from the colons of wild‐type mice and dextran sulphate sodium (DSS)‐induced mice were isolated for high‐throughput RNA‐sequencing. A total of 254 up‐regulated and 1013 down‐regulated mRNAs and 542 up‐regulated and 766 down‐regulated lncRNAs were detected in the DSS group compared with the Control group. Four mRNAs and six lncRNAs were validated by real‐time quantitative PCR. Function analysis showed that dysregulated mRNAs participated in TLR7 signalling pathway, IL‐1 receptor activity, BMP receptor binding and IL‐17 signalling pathway. Furthermore, the possibility of indirect interactions between differentially expressed mRNAs and lncRNAs was illustrated by the competing endogenous RNA (ceRNA) network. LncRNA ENSMUST00000128026 was predicted to bind to mmu‐miR‐6899‐3p, regulating Dnmbp expression. LncRNA NONMMUT143162.1 was predicted to competitively bind to mmu‐miR‐6899‐3p, regulating Tnip3 expression. Finally, the protein‐protein interaction (PPI) network analysis was constructed with 311 nodes and 563 edges. And the highest connectivity degrees were Mmp9, Fpr2 and Ccl3. These results provide novel insights into the functions of lncRNAs and mRNAs involved in the regulation of the intestinal epithelial barrier.
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spelling pubmed-78122592021-01-22 Intestinal epithelial cells related lncRNA and mRNA expression profiles in dextran sulphate sodium‐induced colitis Liu, Huan Li, Teming Zhong, Shizhen Yu, Min Huang, Wenhua J Cell Mol Med Original Articles Intestinal epithelial barrier damage caused by intestinal epithelial cells (IECs) dysfunction plays a crucial role in the pathogenesis and development of inflammatory bowel disease (IBD). Recently, some studies have suggested the emerging role of long non‐coding RNAs (lncRNAs) in IBD. The aim of this study was to reveal lncRNAs and mRNA expression profiles in IECs from a mouse model of colitis and to expand our understanding in the intestinal epithelial barrier regulation. IECs from the colons of wild‐type mice and dextran sulphate sodium (DSS)‐induced mice were isolated for high‐throughput RNA‐sequencing. A total of 254 up‐regulated and 1013 down‐regulated mRNAs and 542 up‐regulated and 766 down‐regulated lncRNAs were detected in the DSS group compared with the Control group. Four mRNAs and six lncRNAs were validated by real‐time quantitative PCR. Function analysis showed that dysregulated mRNAs participated in TLR7 signalling pathway, IL‐1 receptor activity, BMP receptor binding and IL‐17 signalling pathway. Furthermore, the possibility of indirect interactions between differentially expressed mRNAs and lncRNAs was illustrated by the competing endogenous RNA (ceRNA) network. LncRNA ENSMUST00000128026 was predicted to bind to mmu‐miR‐6899‐3p, regulating Dnmbp expression. LncRNA NONMMUT143162.1 was predicted to competitively bind to mmu‐miR‐6899‐3p, regulating Tnip3 expression. Finally, the protein‐protein interaction (PPI) network analysis was constructed with 311 nodes and 563 edges. And the highest connectivity degrees were Mmp9, Fpr2 and Ccl3. These results provide novel insights into the functions of lncRNAs and mRNAs involved in the regulation of the intestinal epithelial barrier. John Wiley and Sons Inc. 2020-12-09 2021-01 /pmc/articles/PMC7812259/ /pubmed/33300279 http://dx.doi.org/10.1111/jcmm.16174 Text en © 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Liu, Huan
Li, Teming
Zhong, Shizhen
Yu, Min
Huang, Wenhua
Intestinal epithelial cells related lncRNA and mRNA expression profiles in dextran sulphate sodium‐induced colitis
title Intestinal epithelial cells related lncRNA and mRNA expression profiles in dextran sulphate sodium‐induced colitis
title_full Intestinal epithelial cells related lncRNA and mRNA expression profiles in dextran sulphate sodium‐induced colitis
title_fullStr Intestinal epithelial cells related lncRNA and mRNA expression profiles in dextran sulphate sodium‐induced colitis
title_full_unstemmed Intestinal epithelial cells related lncRNA and mRNA expression profiles in dextran sulphate sodium‐induced colitis
title_short Intestinal epithelial cells related lncRNA and mRNA expression profiles in dextran sulphate sodium‐induced colitis
title_sort intestinal epithelial cells related lncrna and mrna expression profiles in dextran sulphate sodium‐induced colitis
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7812259/
https://www.ncbi.nlm.nih.gov/pubmed/33300279
http://dx.doi.org/10.1111/jcmm.16174
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