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Identification of differentially expressed miRNAs in the fatty liver of Landes goose (Anser anser)

Unlike mammals, in palmipedes de novo lipogenesis from diet takes place mostly in the liver. The French Landes Goose is famous for its high capacity and susceptibility to fatty liver production. While miRNAs play a critical role in the posttranscriptional regulation of gene expression, miRNAs that a...

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Autores principales: Chen, Fang, Zhang, Hao, Li, Jinjun, Tian, Yong, Xu, Jing, Chen, Li, Wei, Jintao, Zhao, Na, Yang, Xuehai, Zhang, Wei, Lu, Lizhi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5701175/
https://www.ncbi.nlm.nih.gov/pubmed/29176640
http://dx.doi.org/10.1038/s41598-017-16632-7
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author Chen, Fang
Zhang, Hao
Li, Jinjun
Tian, Yong
Xu, Jing
Chen, Li
Wei, Jintao
Zhao, Na
Yang, Xuehai
Zhang, Wei
Lu, Lizhi
author_facet Chen, Fang
Zhang, Hao
Li, Jinjun
Tian, Yong
Xu, Jing
Chen, Li
Wei, Jintao
Zhao, Na
Yang, Xuehai
Zhang, Wei
Lu, Lizhi
author_sort Chen, Fang
collection PubMed
description Unlike mammals, in palmipedes de novo lipogenesis from diet takes place mostly in the liver. The French Landes Goose is famous for its high capacity and susceptibility to fatty liver production. While miRNAs play a critical role in the posttranscriptional regulation of gene expression, miRNAs that are involved in the regulation of goose hepatic steatosis have yet to be elucidated. Using high-throughput sequencing, we analyzed miRNAs expression profile of Landes goose liver after overfeeding for 21 days. Aan-miR-122-5p was the most frequently sequenced known miRNA, but it was unchanged after overfeeding. Compared with normal liver, we identified that 16 conserved miRNAs were up-regulated while the other 9 conserved miRNAs were down-regulated in fatty livers. Many of their predicted target genes played key roles in metabolic pathways leading to the development of hepatic steatosis in the goose by KEGG pathways analysis. ACSL1 and ELOVL6 were critical genes in hepatic lipid metabolism and had opposite expression patterns with aan-miR-203a and aan-miR-125b-5p, respectively. And we validated that aan-miR-203a and aan-miR-125b-5p might involve in the regulation of hepatic lipid metabolism by targeting ACSL1 and ELOVL6, respectively. These results add to our current understanding of the regulation network in goose lipid metabolism.
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spelling pubmed-57011752017-11-30 Identification of differentially expressed miRNAs in the fatty liver of Landes goose (Anser anser) Chen, Fang Zhang, Hao Li, Jinjun Tian, Yong Xu, Jing Chen, Li Wei, Jintao Zhao, Na Yang, Xuehai Zhang, Wei Lu, Lizhi Sci Rep Article Unlike mammals, in palmipedes de novo lipogenesis from diet takes place mostly in the liver. The French Landes Goose is famous for its high capacity and susceptibility to fatty liver production. While miRNAs play a critical role in the posttranscriptional regulation of gene expression, miRNAs that are involved in the regulation of goose hepatic steatosis have yet to be elucidated. Using high-throughput sequencing, we analyzed miRNAs expression profile of Landes goose liver after overfeeding for 21 days. Aan-miR-122-5p was the most frequently sequenced known miRNA, but it was unchanged after overfeeding. Compared with normal liver, we identified that 16 conserved miRNAs were up-regulated while the other 9 conserved miRNAs were down-regulated in fatty livers. Many of their predicted target genes played key roles in metabolic pathways leading to the development of hepatic steatosis in the goose by KEGG pathways analysis. ACSL1 and ELOVL6 were critical genes in hepatic lipid metabolism and had opposite expression patterns with aan-miR-203a and aan-miR-125b-5p, respectively. And we validated that aan-miR-203a and aan-miR-125b-5p might involve in the regulation of hepatic lipid metabolism by targeting ACSL1 and ELOVL6, respectively. These results add to our current understanding of the regulation network in goose lipid metabolism. Nature Publishing Group UK 2017-11-24 /pmc/articles/PMC5701175/ /pubmed/29176640 http://dx.doi.org/10.1038/s41598-017-16632-7 Text en © The Author(s) 2017 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Chen, Fang
Zhang, Hao
Li, Jinjun
Tian, Yong
Xu, Jing
Chen, Li
Wei, Jintao
Zhao, Na
Yang, Xuehai
Zhang, Wei
Lu, Lizhi
Identification of differentially expressed miRNAs in the fatty liver of Landes goose (Anser anser)
title Identification of differentially expressed miRNAs in the fatty liver of Landes goose (Anser anser)
title_full Identification of differentially expressed miRNAs in the fatty liver of Landes goose (Anser anser)
title_fullStr Identification of differentially expressed miRNAs in the fatty liver of Landes goose (Anser anser)
title_full_unstemmed Identification of differentially expressed miRNAs in the fatty liver of Landes goose (Anser anser)
title_short Identification of differentially expressed miRNAs in the fatty liver of Landes goose (Anser anser)
title_sort identification of differentially expressed mirnas in the fatty liver of landes goose (anser anser)
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5701175/
https://www.ncbi.nlm.nih.gov/pubmed/29176640
http://dx.doi.org/10.1038/s41598-017-16632-7
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