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蛋鸡脂肪肝出血综合征对肝脏及腹脂转录组的影响研究OACSTPCD

Effects of fatty liver hemorrhage syndrome on the liver and abdominal fat transcriptomic profile in laying hens

中文摘要英文摘要

旨在鉴定并比较脂肪肝出血综合征(FLHS)蛋鸡肝脏及腹脂组织的转录组特征,揭示FLHS发生发展中肝脏和腹脂调控的关键基因及潜在分子机制,为精确靶向肝脏及腹脂用药提供理论依据.采用高能低蛋白日粮构建蛋鸡FLHS模型,利用转录组测序(RNA-Seq)比较患鸡与正常组肝脏及腹脂基因表达图谱,利用基因本体(GO)功能注释、京都基因组百科全书(KEGG)通路富集和基因集富集分析(GSEA)阐明FLHS蛋鸡肝脏和腹脂差异基因的功能及作用通路;通过反转录PCR(RT-PCR)和RNA-Seq数据验证关键基因的差异表达.结果显示:高能低蛋白日粮可成功诱发蛋鸡FLHS,肝脏和腹脂转录谱发生明显改变.FLHS患鸡肝脏和腹脂中分别有443 个(151 上调表达,292 下调表达)和526个(409 上调表达,117 下调表达)显著差异表达基因(| log2 FC|≥1,P<0.05).富集分析提示,包括磷酸烯醇丙酮酸羧激酶(PCK1)、载脂蛋白a-1(APOA1)在内的肝脏差异基因显著富集于代谢过程和PPAR信号通路而诱发肝脏脂质沉积;白细胞介素 6(IL-6)、细胞因子信号通路抑制因子3(SOCS3)等腹脂差异基因更倾向于参与调控免疫过程和JAK-STAT信号通路导致炎症发生.提示:肝脏和腹脂通过不同途径共同参与蛋鸡FLHS发生发展,特异性靶向干扰肝脏及腹脂间关键差异基因及信号通路,对于优化FLHS的预防及治疗具有重要意义.

This study was to identify and compare the transcriptomic profiles of liver and abdominal fat tissue of laying hens with fatty liver hemorrhage syndrome(FLHS),to reveal the important interaction between liver and abdominal fat,key genes and the underlying mecha-nisms,and to provide theoretical basis for precise targeting of liver and abdominal fat drugs.The FLHS model of laying hens was constructed by high-energy low-protein diet.Then,the gene expression profiles of liver and abdominal fat of FLHS laying hens and normal laying hens were compared by RNA-Seq.GO annotation,KEGG and GSEA pathway enrichment analysis were used to elucidate the critical biological processes and signaling pathways in FLHS pathogenesis enriched by differential genes of liver and abdominal fat from FLHS laying hens.Fi-nally,RT-PCR and RNA-Seq data were employed to verify the differential expressions of the key genes.The results showed that high-ener-gy low-protein diet successfully triggered FLHS in the laying hens with significant alterations of transcription profiles of liver and abdominal fat.By our RNA-seq data,we screened out 443 differential genes(151 upregulated,292 downregulated)and 526 differential genes(409 upregulated,117 downregulated)in liver and abdomen fat,respectively,of FLHS laying hens,as compared with the controls(| log2 FC|≥1,P<0.05).The functionalenrichmentanalysissuggestedthatthedifferentialgenesidentifiedintheliver,including PCK1and APOA1,had a higher enrichment in the metabolic process and the PPAR signaling pathway,accelerating liver lipid deposition.However,IL-6,SOCS3 and other differential genes identified in the abdominal fat exhibited a tendency to be predominantly enriched in the regulation of the immune process and the JAK-STAT signaling pathway,contributing to inflammation.Liver and abdominal fat were both involved and had a critical interaction in the development of FLHS in the laying hens through different pathways.Specific targeted interference of key differential genes and signaling pathways between liver and abdominal fat was of great significance and should be considered to apply to optimizing the prevention and treatment of FLHS.

易昕睿;朱亚玲;马金虎;王毅;王玉洁;朱枚子;李鑫宇;唐云书;薛敏;黄建珍

安徽医科大学基础医学院, 安徽 合肥 230032安徽医科大学基础医学院, 安徽 合肥 230032||安徽医科大学P2 级动物实验中心, 安徽 合肥 230032江西农业大学动物科学技术学院, 江西 南昌 330045

畜牧业

高能低蛋白日粮蛋鸡脂肪肝出血综合征转录组测序差异基因

high-energy low-protein dietlaying hensFLHSRNA-Seqdifferentially expressed genes

《畜牧与兽医》 2024 (002)

37-45 / 9

安徽省科学技术厅省级重点项目(KJ2021A0205);安徽医科大学校级项目(2020xkj007)

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