Regulatory impacts of PPARGC1A gene expression on milk production and cellular metabolism in buffalo mammary epithelial cells

被引:0
|
作者
Hosseini, Seyed Mahdi [1 ]
Ye, Tingzhu [1 ]
Ran, Zaohong [1 ]
Ullah, Farman [1 ]
Liang, Aixin [1 ]
Hua, Guohua [1 ]
Yang, Liguo [1 ]
机构
[1] Huazhong Agr Univ, Natl Ctr Int Res Anim Genet Breeding & Reprod NCIR, Coll Anim Sci & Technol, Wuhan, Peoples R China
关键词
Buffalo; knockdown; mammary epithelial cell; milk; PPARGC1A; FAT SYNTHESIS; MOLECULAR CHARACTERIZATION; BOVINE PPARGC1A; GLAND; POLYMORPHISMS; COACTIVATOR; ASSOCIATION; PGC-1-ALPHA; PROTEINS; STAGE;
D O I
10.1080/10495398.2024.2344210
中图分类号
S8 [畜牧、 动物医学、狩猎、蚕、蜂];
学科分类号
0905 ;
摘要
The PPARGC1A gene plays a fundamental role in regulating cellular energy metabolism, including adaptive thermogenesis, mitochondrial biogenesis, adipogenesis, gluconeogenesis, and glucose/fatty acid metabolism. In a previous study, our group investigated seven SNPs in Mediterranean buffalo associated with milk production traits, and the current study builds on this research by exploring the regulatory influences of the PPARGC1A gene in buffalo mammary epithelial cells (BuMECs). Our findings revealed that knockdown of PPARGC1A gene expression significantly affected the growth of BuMECs, including proliferation, cell cycle, and apoptosis. Additionally, we observed downregulated triglyceride secretion after PPARGC1A knockdown. Furthermore, the critical genes related to milk production, including the STATS, BAD, P53, SREBF1, and XDH genes were upregulated after RNAi, while the FABP3 gene, was downregulated. Moreover, Silencing the PPARGC1A gene led to a significant downregulation of beta-casein synthesis in BuMECs. Our study provides evidence of the importance of the PPARGC1A gene in regulating cell growth, lipid, and protein metabolism in the buffalo mammary gland. In light of our previous research, the current study underscores the potential of this gene for improving milk production efficiency and overall dairy productivity in buffalo populations.
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页数:11
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