scholarly journals Oleic acid stimulates HC11 mammary epithelial cells proliferation and mammary gland development in peripubertal mice through activation of CD36-Ca2+ and PI3K/Akt signaling pathway

Oncotarget ◽  
2018 ◽  
Vol 9 (16) ◽  
pp. 12982-12994 ◽  
Author(s):  
Yingying Meng ◽  
Jing Zhang ◽  
Cong Yuan ◽  
Fenglin Zhang ◽  
Qin Fu ◽  
...  
Keyword(s):  
Oleic Acid ◽  
Mammary Gland ◽  
Epithelial Cells ◽  
Signaling Pathway ◽  
Mammary Gland Development ◽  
Mammary Epithelial Cells ◽  
Akt Signaling ◽  
Mammary Epithelial ◽  
Akt Signaling Pathway ◽  
Gland Development

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.

Lauric Acid Stimulates Mammary Gland Development of Pubertal Mice through Activation of GPR84 and PI3K/Akt Signaling Pathway

2016 ◽  
Vol 65 (1) ◽  
pp. 95-103 ◽  
Author(s):  
Yingying Meng ◽  
Jing Zhang ◽  
Fenglin Zhang ◽  
Wei Ai ◽  
Xiaotong Zhu ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Signaling Pathway ◽  
Lauric Acid ◽  
Mammary Gland Development ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Gland Development

scholarly journals Signal Transducer and Activator of Transcription 5a Mediates Mammary Ductal Branching and Proliferation in the Nulliparous Mouse

Endocrinology ◽  
2010 ◽  
Vol 151 (6) ◽  
pp. 2876-2885 ◽  
Author(s):  
Sarah J. Santos ◽  
Sandra Z. Haslam ◽  
Susan E. Conrad
Keyword(s):  
Mammary Gland ◽  
Epithelial Cells ◽  
Mammary Gland Development ◽  
Kinase Inhibitor ◽  
Mammary Epithelial Cells ◽  
Nuclear Factor Κb ◽  
Mammary Glands ◽  
Mammary Epithelial ◽  
Signal Transducer ◽  
Gland Development

Signal transducer and activator of transcription (Stat)5a is a critical regulator of mammary gland development. Previous studies have focused on Stat5a’s role in the late pregnant and lactating gland, and although active Stat5a is detectable in mammary epithelial cells in virgin mice, little is known about its role during early mammary gland development. In this report, we compare mammary gland morphology in pubertal and adult nulliparous wild-type and Stat5a−/− mice. The Stat5a-null mammary glands exhibited defects in secondary and side branching, providing evidence that Stat5a regulates these processes. In addition, Stat5a−/− mammary glands displayed an attenuated proliferative response to pregnancy levels of estrogen plus progesterone (E+P), suggesting that it plays an important role in early pregnancy. Finally, we examined one potential mediator of Stat5a’s effects, receptor activator of nuclear factor-κB ligand (RANKL). Stat5a−/− mammary glands were defective in inducing RANKL in response to E+P treatment. In addition, regulation of several reported RANKL targets, including inhibitor of DNA binding 2 (Id2), cyclin D1, and the cyclin-dependent kinase inhibitor p21Waf1/Cip1, was altered in Stat5a−/− mammary cells, suggesting that one or more of these proteins mediate the effects of Stat5a in E+P-treated mammary epithelial cells.

scholarly journals Expression of an engrailed-LMO4 fusion protein in mammary epithelial cells inhibits mammary gland development in mice

Oncogene ◽  
2003 ◽  
Vol 23 (8) ◽  
pp. 1507-1513 ◽  
Author(s):  
Ning Wang ◽  
Elena Kudryavtseva ◽  
Irene L Ch'en ◽  
Joshua McCormick ◽  
Tod M Sugihara ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Epithelial Cells ◽  
Fusion Protein ◽  
Mammary Gland Development ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Gland Development

scholarly journals Circ-140/chi-miR-8516/STC1-MMP1 Regulates αs1-/β-Casein Secretion and Lipid Formation in Goat Mammary Epithelial Cells

Genes ◽  
2021 ◽  
Vol 12 (5) ◽  
pp. 671
Author(s):  
Yue Zhang ◽  
Qiong Wu ◽  
Jidan Liu ◽  
Xiaopeng An ◽  
Binyun Cao
Keyword(s):  
Mammary Gland ◽  
Epithelial Cells ◽  
Essential Role ◽  
Mammary Gland Development ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Lipid Formation ◽  
Milk Components ◽  
Gland Development ◽  
Goat Mammary Epithelial Cells

MicroRNAs play an essential role in mammary gland development, and involution is a factor that limits lactation. Chi-miR-8516 is one of the validated microRNAs that regulates the expression of STC1 and MMP1, which surge during the involution of the mammary gland. This study aims to explore the direct or indirect regulation of STC1 and MMP1 by chi-miR-8516 and the regulation of chi-miR-8516 by circ-140. In goat mammary epithelial cells, we found that chi-miR-8516 takes circ-140 as a sponge and regulates MMP1 expression by targeting STC1 and promoting the phosphorylation of MAPK. The examination of αs1-/β-casein and lipid showed the modulation of the circ-140/chi-miR-8516/STC1-MMP1 axis in casein secretion and lipid formation, which was regulated by the phosphorylation of mTOR and STAT5. This study illustrates an axis that regulates the synthesis of milk components, and explores the pathways in which the axis participates.

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