scholarly journals Dietary polyunsaturated fatty acids modulate adipose secretome and is associated with changes in mammary epithelial stem cell self-renewal

2019 ◽  
Vol 71 ◽  
pp. 45-53 ◽  
Author(s):  
Evan M. Hill ◽  
Raymond M. Esper ◽  
Ananda Sen ◽  
Becky R. Simon ◽  
Muhammad N. Aslam ◽  
...  
2018 ◽  
Vol 20 (1) ◽  
Author(s):  
Safiah Olabi ◽  
Ahmet Ucar ◽  
Keith Brennan ◽  
Charles H. Streuli

Shock ◽  
2001 ◽  
Vol 15 (Supplement) ◽  
pp. 73-74
Author(s):  
R. Gillis ◽  
P. Tithof ◽  
N. Neilsen ◽  
M. Barnhill ◽  
R. Andrews ◽  
...  

2011 ◽  
Vol 668 ◽  
pp. e39-e40
Author(s):  
A. Hogenkamp⁎ ◽  
N. van Vlies ◽  
E. van Esch ◽  
A. Fear ◽  
P. Calder ◽  
...  

1993 ◽  
Vol 48 (1) ◽  
pp. 5-15 ◽  
Author(s):  
J.M. Bourre ◽  
M. Bonneil ◽  
M. Clément ◽  
O. Dumont ◽  
G. Durand ◽  
...  

Author(s):  
Melissa McNeil ◽  
Yingying Han ◽  
Peng Sun ◽  
Kazuhide Watanabe ◽  
Jun Jiang ◽  
...  

AbstractMammary gland is an outstanding system to study the regulatory mechanisms governing adult epithelial stem cell activity. Stem cells in the basal layer of the mammary gland fuel the morphogenesis and regeneration of a complex epithelial network during development and upon transplantation. The self-renewal of basal stem/progenitor cells is subjected to regulation by both cell-intrinsic and extrinsic mechanisms. Nfatc1 is a transcription factor that regulates breast tumorigenesis and metastasis, but its role in mammary epithelial development and stem cell function has not been investigated. Here we show that Nfatc1 is expressed in a small subset of mammary basal epithelial cells and its epithelial-specific deletion results in mild defects in side branching and basal-luminal cell balance. Moreover, Nfatc1-deficient basal cells exhibit reduced colony forming ability in vitro and somewhat compromised regenerative potential upon transplantation. Thus, our study provides evidence for a detectable yet non-essential role of Nfatc1 in mammary epithelial morphogenesis and basal stem/progenitor cell self-renewal.


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