scholarly journals Co-expression of estrogen receptor-alpha and targets of estrogen receptor action in proliferating monkey mammary epithelial cells

2006 ◽  
Vol 8 (1) ◽  
Author(s):  
Constantine Dimitrakakis ◽  
Jian Zhou ◽  
Jie Wang ◽  
Ludmila Matyakhina ◽  
Eva Mezey ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Epithelial Cells ◽  
Estrogen Receptor Alpha ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Receptor Alpha ◽  
Receptor Action

scholarly journals Mammary Fat Can Adjust Prolactin Effect on Mammary Epithelial Cells via Leptin and Estrogen

2009 ◽  
Vol 2009 ◽  
pp. 1-8 ◽  
Author(s):  
Yonatan Feuermann ◽  
Sameer J. Mabjeesh ◽  
Avi Shamay
Keyword(s):  
Estrogen Receptor ◽  
Epithelial Cells ◽  
Estrogen Receptor Alpha ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Fat Pad ◽  
Paracrine Factors ◽  
Receptor Alpha ◽  
Mammary Fat Pad ◽  
Aromatase Mrna

Leptin, like estrogen, is one of the endo/paracrine factors, which are synthesized in and secreted from mature adipocytes. The roles of the mammary fat pad and mammary adipocytes in the initiation of lactation are not clear. In this study, we showed that combination of prolactin, leptin and estrogen elevated the expression of the milk protein beta-lactoglobulin. We also showed that after prolactin stimulate the secretion of leptin from the mammary fat, leptin upregulated the expression of estrogen receptor alpha in the mammary epithelial cells. Also, prolactin affected aromatase mRNA expression in the bovine mammary fat and we demonstrated that leptin and prolactin can affect cholesterol secretion from explants in culture to the medium. Therefore, we suggest that prolactin initiates estrogen expression (as represented by aromatase mRNA) in the mammary fat pad, whereas leptin stimulates estrogen receptor alpha expression in the mammary epithelial cells. We hypothesize that leptin and estrogen, secreted from the mammary fat regulate lactation after stimulation of prolactin.

Physiologic estrogen receptor alpha signaling in non-tumorigenic human mammary epithelial cells

2006 ◽  
Vol 99 (1) ◽  
pp. 23-33 ◽  
Author(s):  
Abde M. Abukhdeir ◽  
Brian G. Blair ◽  
Keith Brenner ◽  
Bedri Karakas ◽  
Hiroyuki Konishi ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Epithelial Cells ◽  
Estrogen Receptor Alpha ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Receptor Alpha ◽  
Human Mammary Epithelial Cells ◽  
Human Mammary Epithelial

scholarly journals Cross-talk between Stat5b and estrogen receptor-alpha and -beta in mammary epithelial cells

2001 ◽  
Vol 27 (1) ◽  
pp. 93-106 ◽  
Author(s):  
L Bjornstrom ◽  
E Kilic ◽  
M Norman ◽  
MG Parker ◽  
M Sjoberg
Keyword(s):  
Estrogen Receptor ◽  
Cross Talk ◽  
Estrogen Receptor Alpha ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Epithelial Cell Line ◽  
Receptor Alpha ◽  
Cell Extracts ◽  
C Terminus

Both 17beta-estradiol and prolactin play important roles in the mammary gland, raising the possibility of functional cross-talk between the two signaling pathways. Here, we demonstrate that estrogen receptor-alpha (ERalpha) and -beta (ERbeta) are both able to potentiate transcription from a Stat5-responsive promoter when activated by prolactin. Potentiation was observed not only in the presence of 17beta-estradiol, but also in the presence of anti-estrogens such as tamoxifen and ICI 182,780. The magnitude of the response was dependent on cell-type: in the HC11 mouse mammary epithelial cell line ERbeta potentiates transcription efficiently whereas ERalpha showed low activity. Conversely, in COS-7 cells, both estrogen receptors were active. We show that activation domains in the N-terminus (AF-1) and the C-terminus (AF-2) of the ERs are dispensable for potentiation. The effects are dependent on the presence of an intact DNA-binding/hinge domain, which we show is capable of interacting with Stat5b in vitro and in HC11 cell extracts. We conclude that ERalpha and ERbeta act as coactivators for Stat5b through a mechanism which is independent of AF-1 and AF-2.

scholarly journals Review of: Proliferation of estrogen receptor-alpha-positive mammary epithelial cells is restrained by transforming growth factor-beta1 in adult mice

2006 ◽  
Vol 9 (6) ◽  
pp. 1-3
Author(s):  
H. Kalirai ◽  
R. B. Clarke
Keyword(s):  
Estrogen Receptor ◽  
Growth Factor ◽  
Epithelial Cells ◽  
Estrogen Receptor Alpha ◽  
Transforming Growth Factor ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Transforming Growth Factor Beta1 ◽  
Adult Mice ◽  
Er Alpha

Citation of original article:K. B. Ewan, H. A. Oketch-Rabah, S. A. Ravani, G. Shyamala, H. L. Moses, M. H. Barcellos-Hoff. Proliferation of estrogen receptor-alpha-positive mammary epithelial cells is restrained by transforming growth factor-beta1 in adult mice.American Journal of Pathology2005;167(2): 409–17.Abstract of the original article:Transforming growth factor (TGF)-beta1 is a potent inhibitor of mammary epithelial proliferation. In human breast, estrogen receptor (ER)-alpha cells rarely co-localize with markers of proliferation, but their increased frequency correlates with breast cancer risk. To determine whether TGF-beta1 is necessary for the quiescence of ER-alpha-positive populations, we examined mouse mammary epithelial glands at estrus. Approximately, 35% of epithelial cells showed TGF-beta1 activation, which co-localized with nuclear receptor-phosphorylated Smad 2/3, indicating that TGF-beta signaling is autocrine. Nuclear Smad co-localized with nuclear ER-alpha. To test whether TGF-beta inhibits proliferation, we examined genetically engineered mice with different levels of TGF-beta1. ER-alpha co-localization with markers of proliferation (i.e., Ki-67 or bromodeoxyuridine) at estrus was significantly increased in the mammary glands of TGF-beta1 C57/bl/129SV heterozygote mice. This relationship was maintained after pregnancy but was absent at puberty. Conversely, mammary epithelial expression of constitutively active TGF-beta1 via the MMTV promoter suppressed proliferation of ER-alpha-positive cells. Thus, TGF-beta1 activation functionally restrains ER-alpha-positive cells from proliferating in adult mammary gland. Accordingly, we propose that TGF-beta1 dysregulation may promote proliferation of ER-alpha-positive cells associated with breast cancer risk in humans.

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