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基于基因集富集分析鉴定鸭脂肪肝综合征的关键基因和通路。

Identification of key genes and pathways in duck fatty liver syndrome using gene set enrichment analysis.

机构信息

State Key Laboratory of Swine and Poultry Breeding Industry, Institute of Animal Science, Guangdong Academy of Agricultural Sciences, Key Laboratory of Animal Nutrition and Feed Science in South China, Ministry of Agriculture and Rural Affairs, Guangdong Provincial Key Laboratory of Animal Breeding and Nutrition, Guangzhou 510640, P.R. China.

State Key Laboratory of Swine and Poultry Breeding Industry, Institute of Animal Science, Guangdong Academy of Agricultural Sciences, Key Laboratory of Animal Nutrition and Feed Science in South China, Ministry of Agriculture and Rural Affairs, Guangdong Provincial Key Laboratory of Animal Breeding and Nutrition, Guangzhou 510640, P.R. China; College of Animal Science, Anhui Science and Technology University, Anhui 233100, P.R. China.

出版信息

Poult Sci. 2024 Sep;103(9):104015. doi: 10.1016/j.psj.2024.104015. Epub 2024 Jun 24.

DOI:10.1016/j.psj.2024.104015
PMID:39003797
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11298935/
Abstract

High-laying ducks are often fed high-energy, nutritious feeds to maintain high productivity, which predisposes them to lipid metabolism disorders and the development of fatty liver syndrome (FLS), which seriously affects production performance and has a substantial economic impact on the poultry industry. Therefore, it is necessary to elucidate the mechanisms underlying the development of fatty liver syndrome. In this study, seven Shan Partridge ducks, each with fatty liver syndrome and normal laying ducks, were selected, and Hematoxylin Eosin staining (HE staining), Masson staining, and transcriptome sequencing were performed on liver tissue. In addition to exploring key genes and pathways using conventional analysis methods, we constructed the first Kyoto Encyclopedia of Genes and Genomes (KEGG) database-based predefined gene set containing 12,764 pathways and 16,836 genes and further performed gene set enrichment analysis (GSEA) on the liver transcriptome data. Finally, key nodes and biological processes were identified via the protein-protein interaction (PPI) network. The results showed that the liver in the FL group exhibited steatosis and fibrosis, and a total of 3,663 genes with upregulated expression versus 2,296 downregulated genes were screened by conventional analysis. GSEA analysis and PPI network analysis revealed that the liver in the FL group exhibited disruption of the mitochondrial electron transport chain, leading to decreased oxidative phosphorylation and the secretion of excessive proinflammatory factors amid the continuous accumulation of lipids. Under continuous chronic inflammation, cell cycle arrest triggers apoptosis, while fibrosis becomes more severe, and procarcinogenic genes are activated, leading to the continuous development and deterioration of the liver. In conclusion, the predefined gene set constructed in this study can be used for GSEA, and the identified hub genes provide useful reference data and a solid foundation for the study of the genetic regulatory mechanism of fatty liver syndrome in ducks.

摘要

高产鸭常需投喂高能、高营养饲料以维持高生产性能,这易使它们发生脂质代谢紊乱和脂肪肝综合征(FLS),严重影响生产性能,给家禽业带来巨大经济损失。因此,阐明脂肪肝综合征的发生机制十分必要。本研究选取了 7 只患有脂肪肝综合征的山麻鸭和 7 只正常产蛋鸭,对其肝脏组织进行了苏木精-伊红(HE)染色、Masson 染色和转录组测序。除了使用常规分析方法探索关键基因和通路外,我们还构建了第一个基于京都基因与基因组百科全书(KEGG)数据库的、包含 12764 条通路和 16836 个基因的预定义基因集,并对肝脏转录组数据进行了基因集富集分析(GSEA)。最后,通过蛋白质-蛋白质相互作用(PPI)网络鉴定了关键节点和生物过程。结果表明,FL 组的肝脏发生了脂肪变性和纤维化,通过常规分析共筛选出 3663 个上调基因和 2296 个下调基因。GSEA 分析和 PPI 网络分析表明,FL 组的肝脏中线粒体电子传递链受到破坏,导致氧化磷酸化减少和过量促炎因子的分泌,同时脂质不断积累。在持续的慢性炎症下,细胞周期停滞引发细胞凋亡,而纤维化则变得更加严重,致癌基因被激活,导致肝脏持续发展和恶化。总之,本研究构建的预定义基因集可用于 GSEA,所鉴定的关键基因提供了有用的参考数据和坚实的基础,有助于研究鸭脂肪肝综合征的遗传调控机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43d7/11298935/65b19c2c8445/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43d7/11298935/69a10c6d457b/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43d7/11298935/e854426887f3/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43d7/11298935/e9374ddda08a/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43d7/11298935/2c07006d3664/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43d7/11298935/65b19c2c8445/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43d7/11298935/69a10c6d457b/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43d7/11298935/e854426887f3/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43d7/11298935/e9374ddda08a/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43d7/11298935/2c07006d3664/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43d7/11298935/65b19c2c8445/gr5.jpg

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