Vitamin D Pathway Status and the Identification of Target Genes in the Mouse Mammary Gland

2014 ◽  
Author(s):  
Donald Matthews ◽  
JoEllen Welsh
Keyword(s):  
Vitamin D ◽  
Mammary Gland ◽  
Target Genes ◽  
Mouse Mammary Gland

scholarly journals Glucocorticoid and progesterone inhibit involution and programmed cell death in the mouse mammary gland.

1995 ◽  
Vol 131 (4) ◽  
pp. 1095-1103 ◽  
Author(s):  
Z Feng ◽  
A Marti ◽  
B Jehn ◽  
H J Altermatt ◽  
G Chicaiza ◽  
...  
Keyword(s):  
Cell Death ◽  
Mammary Gland ◽  
Programmed Cell Death ◽  
Hormone Receptors ◽  
Target Genes ◽  
Mouse Mammary Gland ◽  
Binding Activity ◽  
Steroid Hormone Receptors ◽  
Mrna Levels ◽  
Glucocorticoid Hormone

Milk production during lactation is a consequence of the suckling stimulus and the presence of glucocorticoids, prolactin, and insulin. After weaning the glucocorticoid hormone level drops, secretory mammary epithelial cells die by programmed cell death and the gland is prepared for a new pregnancy. We studied the role of steroid hormones and prolactin on the mammary gland structure, milk protein synthesis, and on programmed cell death. Slow-release plastic pellets containing individual hormones were implanted into a single mammary gland at lactation. At the same time the pups were removed and the consequences of the release of hormones were investigated histologically and biochemically. We found a local inhibition of involution in the vicinity of deoxycorticosterone- and progesterone-release pellets while prolactin-release pellets were ineffective. Dexamethasone, a very stable and potent glucocorticoid hormone analogue, inhibited involution and programmed cell death in all the mammary glands. It led to an accumulation of milk in the glands and was accompanied by an induction of protein kinase A, AP-1 DNA binding activity and elevated c-fos, junB, and junD mRNA levels. Several potential target genes of AP-1 such as stromelysin-1, c-jun, and SGP-2 that are induced during normal involution were strongly inhibited in dexamethasone-treated animals. Our results suggest that the cross-talk between steroid hormone receptors and AP-1 previously described in cells in culture leads to an impairment of AP-1 activity and to an inhibition of involution in the mammary gland implying that programmed cell death in the postlactational mammary gland depends on functional AP-1.

scholarly journals Control of TCF-4 Expression by VDR and Vitamin D in the Mouse Mammary Gland and Colorectal Cancer Cell Lines

PLoS ONE ◽  
2009 ◽  
Vol 4 (11) ◽  
pp. e7872 ◽  
Author(s):  
Marcy E. Beildeck ◽  
Md Islam ◽  
Salimuddin Shah ◽  
JoEllen Welsh ◽  
Stephen W. Byers
Keyword(s):  
Colorectal Cancer ◽  
Vitamin D ◽  
Mammary Gland ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Mouse Mammary Gland ◽  
Colorectal Cancer Cell ◽  
Colorectal Cancer Cell Lines

scholarly journals Expression of Notch receptors, ligands, and target genes during development of the mouse mammary gland

2011 ◽  
Vol 226 (7) ◽  
pp. 1940-1952 ◽  
Author(s):  
Ahmed Raafat ◽  
Anita S. Goldhar ◽  
Malgorzata Klauzinska ◽  
Keli Xu ◽  
Idean Amirjazil ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Target Genes ◽  
Mouse Mammary Gland ◽  
Notch Receptors

scholarly journals Estradiol and tamoxifen regulate NRF-1 and mitochondrial function in mouse mammary gland and uterus

2013 ◽  
Vol 51 (2) ◽  
pp. 233-246 ◽  
Author(s):  
Margarita M Ivanova ◽  
Brandie N Radde ◽  
Jieun Son ◽  
Fabiola F Mehta ◽  
Sang-Hyuk Chung ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Target Genes ◽  
Selective Inhibition ◽  
Estrogen Receptor Α ◽  
Mouse Mammary Gland ◽  
Time Dependent ◽  
Nuclear Staining ◽  
Dependent Manner ◽  
Nuclear Respiratory Factor

Nuclear respiratory factor-1 (NRF-1) stimulates the transcription of nuclear-encoded genes that regulate mitochondrial (mt) genome transcription and biogenesis. We reported that estradiol (E2) and 4-hydroxytamoxifen (4-OHT) stimulate NRF-1 transcription in an estrogen receptor α (ERα)- and ERβ-dependent manner in human breast cancer cells. The aim of this study was to determine whether E2and 4-OHT increase NRF-1in vivo. Here, we report that E2and 4-OHT increase NRF-1 expression in mammary gland (MG) and uterus of ovariectomized C57BL/6 mice in a time-dependent manner. E2increased NRF-1 protein in the uterus and MG; however, in MG, 4-OHT increasedNrf1mRNA but not protein. Chromatin immunoprecipitation assays revealed increasedin vivorecruitment of ERα to theNrf1promoter and intron 3 in MG and uterus 6 h after E2and 4-OHT treatment, commensurate with increased NRF-1 expression. E2- and 4-OHT-induced increases in NRF-1 and its target genesTfam,Tfb1m, andTfb2mwere coordinated in MG but not in uterus due to uterine-selective inhibition of the expression of the NRF-1 coactivatorsPpargc1aandPpargc1bby E2and 4-OHT. E2transiently increased NRF-1 and PGC-1α nuclear staining while reducing PGC-1α in uterus. E2, not 4-OHT, activates mt biogenesis in MG and uterus in a time-dependent manner. E2increased mt outer membrane Tomm40 protein levels in MG and uterus whereas 4-OHT increased Tomm40 only in uterus. These data support the hypothesis of tissue-selective regulation of NRF-1 and its downstream targets by E2and 4-OHTin vivo.

Electron microscopic studies on ultrathin frozen sections of lactating mouse mammary gland

1978 ◽  
Vol 36 (2) ◽  
pp. 46-47
Author(s):  
Jan Zarzycki ◽  
Joseph Szroeder
Keyword(s):  
Mammary Gland ◽  
Protein Denaturation ◽  
Chemical Constituents ◽  
Freeze Substitution ◽  
Electron Microscopic Examination ◽  
Mouse Mammary Gland ◽  
Electron Microscopic ◽  
Preparation Methods ◽  
Microscopic Studies ◽  
Ultrathin Frozen Sections

The mammary gland ultrastructure in various functional states is the object of our investigations. The material prepared for electron microscopic examination by the conventional chemical methods has several limitations, the most important are the protein denaturation processes and the loss of large amounts of chemical constituents from the cells. In relevance to this,one can't be sure about a degree the observed images are adequate to the realy ultrastructure of a living cell. To avoid the disadvantages of the chemical preparation methods,some autors worked out alternative physical methods based on tissue freezing / freeze-drying, freeze-substitution, freeze-eatching techniqs/; actually the technique of cryoultraraicrotomy,i,e.cutting ultrathin sections from deep frozen specimens is assented as a complete alternative method. According to the limitations of the routine plastic embbeding methods we were interested to analize the mammary gland ultrastructure during lactation by the cryoultramicrotomy method.

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