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Differentially expressed lncRNAs in liver tissues of TX mice with hepatolenticular degeneration

Wilson's Disease (WD), an ATP7B-mutated inherited disease that affects copper transport, is characterised by liver and nervous system manifestations. Long non-coding (ln-c) RNAs are widely involved in almost all physiological and pathological processes in the body, and are associated with numer...

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Autores principales: Zhang, Juan, Ma, Ying, Xie, Daojun, Bao, Yuancheng, Yang, Wenming, Wang, Han, Jiang, Huaizhou, Han, Hui, Dong, Ting
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7809420/
https://www.ncbi.nlm.nih.gov/pubmed/33446761
http://dx.doi.org/10.1038/s41598-020-80635-0
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author Zhang, Juan
Ma, Ying
Xie, Daojun
Bao, Yuancheng
Yang, Wenming
Wang, Han
Jiang, Huaizhou
Han, Hui
Dong, Ting
author_facet Zhang, Juan
Ma, Ying
Xie, Daojun
Bao, Yuancheng
Yang, Wenming
Wang, Han
Jiang, Huaizhou
Han, Hui
Dong, Ting
author_sort Zhang, Juan
collection PubMed
description Wilson's Disease (WD), an ATP7B-mutated inherited disease that affects copper transport, is characterised by liver and nervous system manifestations. Long non-coding (ln-c) RNAs are widely involved in almost all physiological and pathological processes in the body, and are associated with numerous diseases. The present study aimed to elucidate the lncRNA-mRNA regulation network in a TX WD mouse model using RNA sequencing (RNA-seq). lncRNA expression profiles were screened using RNA-seq and real-time polymerase chain reaction, and differentially expressed lncRNAs and mRNAs were identified. To analyse the biological functions and pathways for the differentially expressed mRNAs, gene ontology and pathway enrichment analyses were performed. A significantly correlated lncRNA-mRNA relationship pair was calculated by CNC analysis to construct differential lncRNA and mRNA co-expression networks. A total of 2564 significantly up-regulated and 1052 down-regulated lncRNAs, and 1576 up-regulated and 297 down-regulated mRNAs, were identified. These genes were found to be associated with key processes such as apoptosis, and KEGG analysis revealed enrichment in the drug metabolism-cytochrome P450 pathway, PPAR signalling pathway, Notch signalling pathway, and MAPK signalling pathway. The identified differential lncRNAs may be involved in the pathogenesis and development of WD liver injury.
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spelling pubmed-78094202021-01-21 Differentially expressed lncRNAs in liver tissues of TX mice with hepatolenticular degeneration Zhang, Juan Ma, Ying Xie, Daojun Bao, Yuancheng Yang, Wenming Wang, Han Jiang, Huaizhou Han, Hui Dong, Ting Sci Rep Article Wilson's Disease (WD), an ATP7B-mutated inherited disease that affects copper transport, is characterised by liver and nervous system manifestations. Long non-coding (ln-c) RNAs are widely involved in almost all physiological and pathological processes in the body, and are associated with numerous diseases. The present study aimed to elucidate the lncRNA-mRNA regulation network in a TX WD mouse model using RNA sequencing (RNA-seq). lncRNA expression profiles were screened using RNA-seq and real-time polymerase chain reaction, and differentially expressed lncRNAs and mRNAs were identified. To analyse the biological functions and pathways for the differentially expressed mRNAs, gene ontology and pathway enrichment analyses were performed. A significantly correlated lncRNA-mRNA relationship pair was calculated by CNC analysis to construct differential lncRNA and mRNA co-expression networks. A total of 2564 significantly up-regulated and 1052 down-regulated lncRNAs, and 1576 up-regulated and 297 down-regulated mRNAs, were identified. These genes were found to be associated with key processes such as apoptosis, and KEGG analysis revealed enrichment in the drug metabolism-cytochrome P450 pathway, PPAR signalling pathway, Notch signalling pathway, and MAPK signalling pathway. The identified differential lncRNAs may be involved in the pathogenesis and development of WD liver injury. Nature Publishing Group UK 2021-01-14 /pmc/articles/PMC7809420/ /pubmed/33446761 http://dx.doi.org/10.1038/s41598-020-80635-0 Text en © The Author(s) 2021 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Zhang, Juan
Ma, Ying
Xie, Daojun
Bao, Yuancheng
Yang, Wenming
Wang, Han
Jiang, Huaizhou
Han, Hui
Dong, Ting
Differentially expressed lncRNAs in liver tissues of TX mice with hepatolenticular degeneration
title Differentially expressed lncRNAs in liver tissues of TX mice with hepatolenticular degeneration
title_full Differentially expressed lncRNAs in liver tissues of TX mice with hepatolenticular degeneration
title_fullStr Differentially expressed lncRNAs in liver tissues of TX mice with hepatolenticular degeneration
title_full_unstemmed Differentially expressed lncRNAs in liver tissues of TX mice with hepatolenticular degeneration
title_short Differentially expressed lncRNAs in liver tissues of TX mice with hepatolenticular degeneration
title_sort differentially expressed lncrnas in liver tissues of tx mice with hepatolenticular degeneration
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7809420/
https://www.ncbi.nlm.nih.gov/pubmed/33446761
http://dx.doi.org/10.1038/s41598-020-80635-0
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