miR-375 Induced the Formation and Transgenerational Inheritance of Fatty Liver in Poultry by Targeting MAP3K1.

IF 2.6 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
Heng-li Xie, Yonghong Zhang, Xiaoyang Tan, Yi Zheng, Hongyu Ni, Lijie Dong, Jinlei Zheng, Jinfu Diao, Yijing Yin, Jiabao Zhang, Xuefeng Sun, Yuwei Yang
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Abstract

The liver of poultry is the primary site of lipid synthesis. The excessive production of lipids accumulates in liver tissues causing lipid metabolism disorders, which result in fatty liver disease and have a transgenerational effect of acquired phenotypes. However, its specific mechanisms have not yet been fully understood. In this study, the differentially expressed miR-375 as well as its target gene MAP3K1 (mitogen-activated protein kinase kinase kinase 1) were screened out by interaction network analysis of microRNA sequencing results and transcriptome profiling in the fatty liver group of the F0-F3 generation (p < 0.05 or p < 0.01). Furthermore, the results showed that the number of lipid droplets and triglyceride content were significantly decreased after upregulation of miR-375 in primary hepatocyte culture in vitro (p < 0.05 or p < 0.01). The MAP3K1 knockdown group exhibited the opposite trends (p < 0.05 or p < 0.01). P53, Bcl-x, PMP22, and CDKN2C related to cell proliferation were significantly upregulated or downregulated after knocking down MAP3K1 (p < 0.05). This research uniquely revealed that silencing miR-375 inhibits lipid biosynthesis and promotes cell proliferation, which may be due to the partial regulation of the expression level of MAP3K1, thereby further participating in the transgenerational inheritance process of regulating liver lipid metabolism. These results reveal the pathogenesis of fatty liver in noncoding RNA and provide good candidate genes for breeding progress of disease resistance in chickens.
miR-375通过靶向MAP3K1诱导家禽脂肪肝的形成和跨代遗传。
家禽的肝脏是脂质合成的主要部位。脂质的过量产生在肝组织中积累,导致脂质代谢紊乱,从而导致脂肪肝疾病,并具有获得性表型的跨代效应。然而,其具体机制尚未完全了解。本研究通过对F0-F3代脂肪肝组microRNA测序结果的相互作用网络分析和转录组分析,筛选出差异表达的miR-375及其靶基因MAP3K1(丝裂原活化蛋白激酶激酶激酶1)(p < 0.05或p < 0.01)。此外,结果显示,在体外培养的原代肝细胞中,上调miR-375后,脂滴数量和甘油三酯含量显著降低(p < 0.05或p < 0.01)。MAP3K1敲低组表现出相反的趋势(p < 0.05或p < 0.01)。敲低MAP3K1后,与细胞增殖相关的P53、Bcl-x、PMP22、CDKN2C均显著上调或下调(p < 0.05)。本研究独特地揭示了沉默miR-375可抑制脂质生物合成,促进细胞增殖,这可能是由于部分调控MAP3K1的表达水平,从而进一步参与调节肝脏脂质代谢的跨代遗传过程。这些结果揭示了非编码RNA中脂肪肝的发病机制,为鸡抗病育种提供了良好的候选基因。
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来源期刊
DNA and cell biology
DNA and cell biology 生物-生化与分子生物学
CiteScore
6.60
自引率
0.00%
发文量
93
审稿时长
1.5 months
期刊介绍: DNA and Cell Biology delivers authoritative, peer-reviewed research on all aspects of molecular and cellular biology, with a unique focus on combining mechanistic and clinical studies to drive the field forward. DNA and Cell Biology coverage includes: Gene Structure, Function, and Regulation Gene regulation Molecular mechanisms of cell activation Mechanisms of transcriptional, translational, or epigenetic control of gene expression Molecular Medicine Molecular pathogenesis Genetic approaches to cancer and autoimmune diseases Translational studies in cell and molecular biology Cellular Organelles Autophagy Apoptosis P bodies Peroxisosomes Protein Biosynthesis and Degradation Regulation of protein synthesis Post-translational modifications Control of degradation Cell-Autonomous Inflammation and Host Cell Response to Infection Responses to cytokines and other physiological mediators Evasive pathways of pathogens.
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