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Circadian Gene PER2 Silencing Downregulates PPARG and SREBF1 and Suppresses Lipid Synthesis in Bovine Mammary Epithelial Cells

文献类型： 外文期刊

作者： Jing, Yujia 1 ; Chen, Yifei 2 ; Wang, Shan 2 ; Ouyang, Jialiang 2 ; Hu, Liangyu 2 ; Yang, Qingyong 1 ; Wang, Mengzhi 2 ; Zhang, Bin 1 ; Loor, Juan J. 3 ;

作者机构： 1.Xinjiang Acad Agr Reclamat Sci, State Key Lab Sheep Genet Improvement & Hlth Prod, Shihezi 832000, Peoples R China

2.Yangzhou Univ, Coll Anim Sci & Technol, Yangzhou 225009, Jiangsu, Peoples R China

3.Univ Illinois, Dept Anim Sci, 328 Mumford Hall, Urbana, IL 61801 USA

4.Univ Illinois, Div Nutr Sci, Urbana, IL 61801 USA

关键词： clock signaling; milk fat; lactation; transcription

期刊名称：BIOLOGY-BASEL （ 影响因子：5.168； ）

ISSN：

年卷期： 2021 年 10 卷 12 期

页码：

收录情况： SCI

摘要： Simple Summary The present study was constructed to determine the effects of the core circadian clock gene, Period 2 (PER2), on lipid synthesis in bovine mammary epithelial cells (BMECs). Data revealed that PER2-regulated genes were involved in fatty acid de novo synthesis, desaturation, TAG accumulation, and lipid droplet secretion in primary BMECs, partly by inhibiting PPARG and SREBF1. Our overall data suggests that PER2 in bovine mammary cells plays a role in regulating milk fat synthesis directly, or via the activation of the transcription regulators PPARG and SREBF1. This study provides molecular evidence underscoring a link between the circadian clock and lipid metabolism in bovines. PER2, a circadian clock gene, is associated with mammary gland development and lipid synthesis in rodents, partly via regulating peroxisome proliferator-activated receptor gamma (PPARG). Whether such a type of molecular link existed in bovines was unclear. We hypothesized that PER2 was associated with lipid metabolism and regulated cell cycles and apoptosis in bovine mammary epithelial cells (BMECs). To test this hypothesis, BMECs isolated from three mid-lactation (average 110 d postpartum) cows were used. The transient transfection of small interfering RNA (siRNA) was used to inhibit PER2 transcription in primary BMECs. The silencing of PER2 led to lower concentrations of cellular lipid droplets and triacylglycerol along with the downregulation of lipogenic-related genes such as ACACA, FASN, LPIN1, and SCD, suggesting an overall inhibition of lipogenesis and desaturation. The downregulation of PPARG and SREBF1 in response to PER2 silencing underscored the importance of circadian clock signaling and the transcriptional regulation of lipogenesis. Although the proliferation of BMECs was not influenced by PER2 silencing, the number of cells in the G2/GM phase was upregulated. PER2 silencing did not affect cell apoptosis. Overall, the data provided evidence that PER2 participated in the coordination of mammary lipid metabolism and was potentially a component of the control of lipid droplets and TAG synthesis in ruminant mammary cells. The present data suggested that such an effect could occur through direct effects on transcriptional regulators.

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