Protein 14-3-3ε Regulates Cell Proliferation and Casein Synthesis via PI3K-mTOR Pathway in Dairy Cow Mammary Epithelial Cells

2018 ◽  
Vol 66 (45) ◽  
pp. 12000-12008 ◽  
Author(s):  
Mengyu Wang ◽  
Zekun Wang ◽  
Chao Yang ◽  
Liu Liu ◽  
Nan Jiang
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cells ◽  
Dairy Cow ◽  
Mammary Epithelial Cells ◽  
Mtor Pathway ◽  
Mammary Epithelial ◽  
Casein Synthesis

Septin6 regulates cell growth and casein synthesis in dairy cow mammary epithelial cells via mTORC1 pathway

2019 ◽  
Vol 86 (2) ◽  
pp. 181-187
Author(s):  
Bin Li ◽  
Zhuzha Basang ◽  
Lijun Hu ◽  
Liu Liu ◽  
Nan Jiang
Keyword(s):  
Cell Growth ◽  
Epithelial Cells ◽  
Dairy Cow ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Regulatory Factor ◽  
Mtor Inhibition ◽  
Mtorc1 Pathway ◽  
Positive Factor ◽  
Casein Synthesis

AbstractThis research paper addresses the hypothesis that Septin6 is a key regulatory factor influencing amino acid (AA)-mediated cell growth and casein synthesis in dairy cow mammary epithelial cells (DCMECs). DCMECs were treated with absence of AA (AA−), restricted concentrations of AA (AAr) or normal concentrations of AA (AA+) for 24 h. Cell growth, expression of CSN2 and Septin6 were increased in response to AA supply. Overexpressing or inhibiting Septin6 demonstrated that cell growth, expression of CSN2, mTOR, p-mTOR, S6K1 and p-S6K1 were up-regulated by Septin6. Furthermore, overexpressing or inhibiting mTOR demonstrated that the increase in cell growth and expression of CSN2 in response to Septin6 overexpression were inhibited by mTOR inhibition, and vice versa. Our hypothesis was supported; we were able to show that Septin6 is an important positive factor for cell growth and casein synthesis, it up-regulates AA-mediated cell growth and casein synthesis through activating mTORC1 pathway in DCMECs.

RagD regulates amino acid mediated-casein synthesis and cell proliferation via mTOR signalling in cow mammary epithelial cells

2018 ◽  
Vol 85 (2) ◽  
pp. 204-211 ◽  
Author(s):  
Ying Mu ◽  
Dongmei Zheng ◽  
Cong Wang ◽  
Wei Yu ◽  
Xiaonan Zhang
Keyword(s):  
Cell Proliferation ◽  
Amino Acid ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Mammary Tissue ◽  
Lactation Period ◽  
Mtor Inhibition ◽  
Pregnancy And Lactation ◽  
Casein Synthesis

This research paper addresses the hypothesis that RagD is a key signalling factor that regulates amino acid (AA) mediated-casein synthesis and cell proliferation in cow mammary epithelial cells (CMECs). The expression of RagD was analysed at different times during pregnancy and lactation in bovine mammary tissue from dairy cows. We showed that expression of RagD at lactation period was higher (P < 0·05) than that at pregnancy period. When CMECs were treated with methionine (Met) or lysine (Lys), expression of RagD, β-casein (CSN2), mTOR and p-mTOR, and cell proliferation were increased. Further, when CMECs were treated to overexpress RagD, expression of CSN2, mTOR and p-mTOR, and cell proliferation were up-regulated. Furthermore, the increase in expression of CSN2, mTOR and p-mTOR, and cell proliferation in response to Met or Lys supply was inhibited by inhibiting RagD, and those effects were reversed in the overexpression model. When CMECs were treated with RagD overexpression together with mTOR inhibition or conversely with RagD inhibition together with mTOR overexpression, results showed that the increase in expression of CSN2 and cell proliferation in response to RagD overexpression was prevented by inhibiting mTOR, and those effects were reversed by overexpressing mTOR. The interaction of RagD with subunit proteins of mTORC1 was analysed, and the result showed that RagD interacted with Raptor. CMECs were treated with Raptor inhibition, and the result showed that the increase in expression of mTOR and p-mTOR in response to RagD overexpression was inhibited by inhibiting Raptor.In conclusion, our study showed that RagD is an important activation factor of mTORC1 in CMECs, activating AA-mediated casein synthesis and cell proliferation, potentially acting via Raptor.

14-3-3γ affects mTOR pathway and regulates lactogenesis in dairy cow mammary epithelial cells

2015 ◽  
Vol 51 (7) ◽  
pp. 697-704 ◽  
Author(s):  
Nagam Khudhair ◽  
Chaochao Luo ◽  
Ahmed Khalid ◽  
Li Zhang ◽  
Shuang Zhang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Dairy Cow ◽  
Mammary Epithelial Cells ◽  
Mtor Pathway ◽  
Mammary Epithelial

Mitochondrial ATAD3A regulates milk biosynthesis and proliferation of mammary epithelial cells from dairy cow via the mTOR pathway

2018 ◽  
Vol 42 (5) ◽  
pp. 533-542 ◽  
Author(s):  
Dongying Chen ◽  
Xiaohan Yuan ◽  
Lijie Liu ◽  
Minghui Zhang ◽  
Bo Qu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Dairy Cow ◽  
Mammary Epithelial Cells ◽  
Mtor Pathway ◽  
Mammary Epithelial

Liver X receptor α participates in LPS-induced reduction of triglyceride synthesis in bovine mammary epithelial cells

2020 ◽  
pp. 1-7
Author(s):  
Jianfa Wang ◽  
Shuai Lian ◽  
Jun Song ◽  
Hai Wang ◽  
Xu Zhang ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Epithelial Cells ◽  
Dairy Cow ◽  
Milk Fat ◽  
Mammary Epithelial Cells ◽  
Liver X Receptor ◽  
Mammary Epithelial ◽  
Triglyceride Synthesis ◽  
Milk Fat Depression ◽  
Liver X Receptor Α

Abstract Lipopolysaccharides (LPS) could induce milk fat depression via regulating the body and blood fat metabolism. However, it is not completely clear how LPS might regulate triglyceride synthesis in dairy cow mammary epithelial cells (DCMECs). DCMECs were isolated and purified from dairy cow mammary tissue and treated with LPS. The level of triglyceride synthesis, the expression and activity of the liver X receptor α (LXRα), enzymes related to de novo fatty acid synthesis, and the expression of the fatty acid transporters were investigated. We found that LPS decreased the level of triglyceride synthesis via a down-regulation of the transcription, translation, and nuclear translocation level of the LXRα. The results also indicated that the transcription level of the LXRα target genes, sterol regulatory element binding protein 1 (SREBP1), fatty acid synthetase (FAS), acetyl-CoA carboxylase-1 (ACC1), were significantly down-regulated in DCMECs after LPS treatment. Our data may provide new insight into the mechanisms of milk fat depression caused by LPS.

scholarly journals p19ARFDetermines the Balance between Normal Cell Proliferation Rate and Apoptosis during Mammary Gland Development

2004 ◽  
Vol 15 (5) ◽  
pp. 2302-2311 ◽  
Author(s):  
Yijun Yi ◽  
Anne Shepard ◽  
Frances Kittrell ◽  
Biserka Mulac-Jericevic ◽  
Daniel Medina ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Mammary Gland ◽  
Epithelial Cells ◽  
Protein Level ◽  
Normal Cell ◽  
Mammary Gland Development ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Proliferation Rate ◽  
Gland Development

This study demonstrated, for the first time, the following events related to p19ARFinvolvement in mammary gland development: 1) Progesterone appears to regulate p19ARFin normal mammary gland during pregnancy. 2) p19ARFexpression levels increased sixfold during pregnancy, and the protein level plateaus during lactation. 3) During involution, p19ARFprotein level remained at high levels at 2 and 8 days of involution and then, declined sharply at day 15. Absence of p19ARFin mammary epithelial cells leads to two major changes, 1) a delay in the early phase of involution concomitant with downregulation of p21Cip1and decrease in apoptosis, and 2) p19ARFnull cells are immortal in vivo measured by serial transplantion, which is partly attributed to complete absence of p21Cip1compared with WT cells. Although, p19ARFis dispensable in mammary alveologenesis, as evidenced by normal differentiation in the mammary gland of pregnant p19ARFnull mice, the upregulation of p19ARFby progesterone in the WT cells and the weakness of p21Cip1in mammary epithelial cells lacking p19ARFstrongly suggest that the functional role(s) of p19ARFin mammary gland development is critical to sustain normal cell proliferation rate during pregnancy and normal apoptosis in involution possibly through the p53-dependent pathway.

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