scholarly journals Mammary adipocytes bioactivate 25-hydroxyvitamin D3 and signal via vitamin D3 receptor, modulating mammary epithelial cell growth

2011 ◽  
Vol 112 (11) ◽  
pp. 3393-3405 ◽  
Author(s):  
Stephen Ching ◽  
Soumya Kashinkunti ◽  
Matthew D. Niehaus ◽  
Glendon M. Zinser
Keyword(s):  
Cell Growth ◽  
Epithelial Cell ◽  
Vitamin D3 ◽  
Mammary Epithelial Cell ◽  
Mammary Epithelial ◽  
D3 Receptor ◽  
Vitamin D3 Receptor

Nulliparous CCAAT/Enhancer Binding Proteinδ (C/EBPδ) Knockout Mice Exhibit Mammary Gland Ductal Hyperlasia

2003 ◽  
Vol 228 (3) ◽  
pp. 278-285 ◽  
Author(s):  
Andrew P. Gigliotti ◽  
Peter F. Johnson ◽  
Esta Sterneck ◽  
James W. DeWille
Keyword(s):  
Mammary Gland ◽  
Cell Growth ◽  
Epithelial Cell ◽  
Mammary Epithelial Cell ◽  
Mammary Epithelial Cells ◽  
Growth Control ◽  
Mammary Epithelial ◽  
Estrus Cycle ◽  
The Mean ◽  
Cell Growth Control

CCAAT/Enhancer binding proteins (C/EBPs) are a family of nuclear proteins that function in the control of cell growth, death, and differentiation. We previously reported that C/EBPδ plays a key role in mammary epithelial cell G0 growth arrest. In this report, we investigated the role of C/EBPδ in mammary gland development and function using female mice homozygous for a targeted deletion of C/EBPδ (C/EBPδ –/–). C/EBPδ –/– females develop normally and exhibit normal reproductive and lactational performance. Adult nulliparous C/EBPδ –/– females, however, exhibit mammary epithelial cell growth control defects. The mean number of mammary ductal branches is significantly higher in adult nulliparous C/EBPδ –/– females compared with C/EBPδ +/+ (wild-type control) females (66.8 ± 5.2 vs 42.9 * 6.3 branch points/field, P < 0.01). In addition, the mean total mammary gland cellular volume occupied by epithelium is significantly higher in adult nulliparous C/EBPδ –/– females compared with C/EBPδ +/+ controls (29.0± 1.4 vs 20.4 ± 1.3, P < 0.001). Our results showed that the BrdU labeling index was significantly higher in mammary epithelial cells from nulliparous C/EBPδ –/– females compared with C/EBPδ +/+ controls during the proestrus/estrus (4.55 ± 0.70 vs 2.14 ± 0.43, P < 0.01) and metestrus/diestrus (6.92 ± 0.75 vs 3.98 ± 0.43 P < 0.01) phases of the estrus cycle. In contrast, the percentage of mammary epithelial cells undergoing apoptosis during both phases of the estrus cycle did not differ between C/EBPδ –/– and C/EBPδ +/+ females. The increased epithelial cell content and proliferative capacity was restricted to the nulliparous C/EBPδ –/– females as no differences in mammary gland morphology, ductal branching or total epithelial content were observed between multiparous C/EBPδ –/– and C/EBPδ +/+ females. These results demonstrate that C/EBPδ plays a novel role in mammary epithelial cell growth control that appears to be restricted to the nulliparous mammary gland.

Regulation of Mammary Epithelial Cell Growth in Mice and Rats*

1990 ◽  
Vol 11 (4) ◽  
pp. 494-523 ◽  
Author(s):  
WALTER IMAGAWA ◽  
GAUTAM K. BANDYOPADHYAY ◽  
SATYABRATA NANDI
Keyword(s):  
Cell Growth ◽  
Epithelial Cell ◽  
Mammary Epithelial Cell ◽  
Mammary Epithelial

scholarly journals CLOCK regulates mammary epithelial cell growth and differentiation

2016 ◽  
Vol 311 (6) ◽  
pp. R1125-R1134 ◽  
Author(s):  
Theresa Casey ◽  
Jennifer Crodian ◽  
Aridany Suárez-Trujillo ◽  
Emily Erickson ◽  
Bethany Weldon ◽  
...  
Keyword(s):  
Cell Growth ◽  
Epithelial Cell ◽  
Mammary Epithelial Cell ◽  
Mammary Epithelial ◽  
Serum Starvation ◽  
Epithelial Cell Line ◽  
Wild Type ◽  
Physiological Processes ◽  
Qpcr Analysis ◽  
Cell Growth And Differentiation

Circadian clocks influence virtually all physiological processes, including lactation. Here, we investigate the role of the CLOCK gene in regulation of mammary epithelial cell growth and differentiation. Comparison of mammary morphology in late-pregnant wild-type and ClockΔ19 mice, showed that gland development was negatively impacted by genetic loss of a functional timing system. To understand whether these effects were due, in part, to loss of CLOCK function in the gland, the mouse mammary epithelial cell line, HC11, was transfected with short hairpin RNA that targeted Clock (shClock). Cells transfected with shClock expressed 70% less Clock mRNA than wild-type (WT) HC11 cultures, which resulted in significantly depressed levels of CLOCK protein ( P < 0.05). HC11 lines carrying shClock had four-fold higher growth rates ( P < 0.05), and the percentage of cells in G1 phase was significantly higher (90.1 ± 1.1% of shClock vs. 71.3 ± 3.6% of WT-HC11) following serum starvation. Quantitative-PCR (qPCR) analysis showed shClock had significant effects ( P < 0.0001) on relative expression levels of Ccnd1, Wee1, and Tp63. qPCR analysis of the effect of shClock on Fasn and Cdh1 expression in undifferentiated cultures and cultures treated 96 h with dexamethasone, insulin, and prolactin (differentiated) found levels were reduced by twofold and threefold, respectively ( P < 0.05), in sh Clock line relative to WT cultures. Abundance of CDH1 and TP63 proteins were significantly reduced in cultures transfected with sh Clock. These data support how CLOCK plays a role in regulation of epithelial cell growth and differentiation in the mammary gland.

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