Developmental and Hormonal Regulation of Wnt Gene Expression in the Mouse Mammary Gland

1995 ◽  
pp. 105-106
Author(s):  
Stephen Weber-Hall ◽  
Deborah Phippard ◽  
Christina Niemeyer ◽  
Trevor Dale
Keyword(s):  
Gene Expression ◽  
Mammary Gland ◽  
Hormonal Regulation ◽  
Mouse Mammary Gland

Hormonal regulation of mitochondrial Tim23 gene expression in the mouse mammary gland

2001 ◽  
Vol 172 (1-2) ◽  
pp. 177-184 ◽  
Author(s):  
Y. Sun ◽  
T. Kuraishi ◽  
F. Aoki ◽  
S. Sakai
Keyword(s):  
Gene Expression ◽  
Mammary Gland ◽  
Hormonal Regulation ◽  
Mouse Mammary Gland

Developmental and hormonal regulation of Wnt gene expression in the mouse mammary gland

1994 ◽  
Vol 57 (3) ◽  
pp. 205-214 ◽  
Author(s):  
Stephen J. Weber-Hall ◽  
Deborah J. Phippard ◽  
Christina C. Niemeyer ◽  
Trevor C. Dale
Keyword(s):  
Gene Expression ◽  
Mammary Gland ◽  
Hormonal Regulation ◽  
Mouse Mammary Gland

Corticosterone is required for the prolactin receptor gene expression in the late pregnant mouse mammary gland

1997 ◽  
Vol 132 (1-2) ◽  
pp. 177-183 ◽  
Author(s):  
Yasushi Mizoguchi ◽  
Hirohito Yamaguchi ◽  
Fugaku Aoki ◽  
Jumpei Enami ◽  
Senkiti Sakai
Keyword(s):  
Gene Expression ◽  
Mammary Gland ◽  
Receptor Gene ◽  
Prolactin Receptor ◽  
Pregnant Mouse ◽  
Mouse Mammary Gland ◽  
Prolactin Receptor Gene ◽  
Receptor Gene Expression

Regulated expression and growth inhibitory effects of transforming growth factor-beta isoforms in mouse mammary gland development

Development ◽  
1991 ◽  
Vol 113 (3) ◽  
pp. 867-878 ◽  
Author(s):  
S.D. Robinson ◽  
G.B. Silberstein ◽  
A.B. Roberts ◽  
K.C. Flanders ◽  
C.W. Daniel
Keyword(s):  
Gene Expression ◽  
Mammary Gland ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Slow Release ◽  
Mouse Mammary Gland ◽  
Tgf Beta ◽  
Growth Factor Beta ◽  
Beta 2

Transforming Growth Factor-beta 1 (TGF-beta 1) was previously shown to inhibit reversibly the growth of mouse mammary ducts when administered in vivo by miniature slow-release plastic implants. We now report a comparative analysis of three TGF-beta isoforms with respect to gene expression and localization of protein products within the mouse mammary gland. Our studies revealed overlapping expression patterns of TGF-beta 1, TGF-beta 2 and TGF-beta 3 within the epithelium of the actively-growing mammary end buds during branching morphogenesis, as well as within the epithelium of growth-quiescent ducts. However, TGF-beta 3 was the only isoform detected in myoepithelial progenitor cells (cap cells) of the growing end buds and myoepithelial cells of the mature ducts. During pregnancy, TGF-beta 2 and TGF-beta 3 transcripts increased to high levels, in contrast to TGF-beta 1 transcripts which were moderately abundant; TGF-beta 2 was significantly transcribed only during pregnancy. Molecular hybridization in situ revealed overlapping patterns of expression for the three TGF-beta isoforms during alveolar morphogenesis, but showed that, in contrast to the patterns of TGF-beta 1 and TGF-beta 2 expression, TGF-beta 3 is expressed more heavily in ducts than in alveoli during pregnancy. Developing alveolar tissue and its associated ducts displayed striking TGF-beta 3 immunoreactivity which was greatly reduced during lactation. All three isoforms showed dramatically reduced expression in lactating tissue. The biological effects of active, exogenous TGF-beta 2 and TGF-beta 3 were tested with slow-release plastic implants. These isoforms, like TGF-beta 1, inhibited mammary ductal elongation in situ by causing the disappearance of the proliferating stem cell layer (cap cells) and rapid involution of ductal end buds. None of the isoforms were active in inhibiting alveolar morphogenesis. We conclude that under the limited conditions of these tests, the three mammalian isoforms are functionally equivalent. However, striking differences in patterns of gene expression and in the distribution of immunoreactive peptides suggest that TGF-beta isoforms may have distinct roles in mammary growth regulation, morphogenesis and functional differentiation.

Developmental expression of pIgR gene in sheep mammary gland and hormonal regulation

2002 ◽  
Vol 69 (1) ◽  
pp. 13-26 ◽  
Author(s):  
AURORE RINCHEV-ALARNOLD ◽  
LUCETTE BELAIR ◽  
JEAN DJIANE
Keyword(s):  
Gene Expression ◽  
Mammary Gland ◽  
Hormonal Regulation ◽  
Mrna Level ◽  
Immunohistochemical Analysis ◽  
Developmental Expression ◽  
Secretory Iga ◽  
Mrna Levels ◽  
Immunoglobulin Receptor ◽  
Pregnancy And Lactation

Secretory IgA found in external secretions are constituted by polymeric IgA (pIgA) bound to the extra-cellular part of the polymeric immunoglobulin receptor (pIgR). The receptor mediates transcytosis of pIgA across epithelial cells. The aim of the present study was to analyse the evolution of pIgR expression in the sheep mammary gland during the development of the mammary gland and to analyse its hormonal regulation. Gene expression of the pIgR was analysed in sheep mammary gland during pregnancy and lactation. By Northern Blot analysis, we observed that low levels of pIgR mRNA are expressed until day 70 of pregnancy. Accumulation of pIgR mRNA started during the third part of pregnancy and intensified 3 d after parturition to reach highest levels during established lactation (day 70). In situ hybridization analysis was used to confirm the increase in pIgR gene expression per mammary epithelial cell. In order to examine the hormonal regulation of the pIgR expression, virgin ewes were hormonally treated. Treatment with oestradiol and progesterone increased pIgR mRNA levels slightly. Subsequent addition of glucocorticoids induced a significant accumulation of pIgR mRNA in the mammary gland of the treated animals. Immunohistochemical analysis was performed to verify that the increase of pIgR mRNA level was associated with enhancement of the pIgR protein in mammary cells. No increase of pIgR mRNA levels were observed if PRL secretion was blocked by bromocryptine injections throughout the hormonal procedure. In conclusion, the present experiments suggest that the enhancement of pIgR levels during lactation result from combined effects of both prolactin and glucocorticoids.

Gene expression and hormonal regulation of adiponectin and its receptors in bovine mammary gland and mammary epithelial cells

2010 ◽  
Vol 82 (1) ◽  
pp. 99-106 ◽  
Author(s):  
Yoshihisa OHTANI ◽  
Tomo YONEZAWA ◽  
Sang-Houn SONG ◽  
Tatsuyuki TAKAHASHI ◽  
Astrid ARDIYANTI ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mammary Gland ◽  
Epithelial Cells ◽  
Hormonal Regulation ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Bovine Mammary Gland

scholarly journals Calcitriol and Its Analogs Establish the Immunosuppressive Microenvironment That Drives Metastasis in 4T1 Mouse Mammary Gland Cancer

2018 ◽  
Vol 19 (7) ◽  
pp. 2116 ◽  
Author(s):  
Agata Pawlik ◽  
Artur Anisiewicz ◽  
Beata Filip-Psurska ◽  
Marcin Nowak ◽  
Eliza Turlej ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mammary Gland ◽  
Lymph Nodes ◽  
Expression Analysis ◽  
Gene Expression Analysis ◽  
Cancer Metastasis ◽  
Transforming Growth Factor ◽  
Mouse Mammary Gland ◽  
Th2 Response ◽  
Mammary Gland Cancer

In our previous study, calcitriol and its analogs PRI-2191 and PRI-2205 stimulated 4T1 mouse mammary gland cancer metastasis. Therefore, we aimed to analyze the inflammatory response in 4T1-bearing mice treated with these compounds. Gene expression analysis of the splenocytes and regional lymph nodes demonstrated prevalence of the T helper lymphocytes (Th2) response with an increased activity of regulatory T (Treg) lymphocytes in mice treated with these compounds. We also observed an increased number of mature granulocytes and B lymphocytes and a decreased number of TCD4+, TCD4+CD25+, and TCD8+, as well as natural killer (NK) CD335+, cells in the blood of mice treated with calcitriol and its analogs. Among the splenocytes, we observed a significant decrease in NK CD335+ cells and an increase in TCD8+ cells. Calcitriol and its analogs decreased the levels of interleukin (IL)-1β and IL-10 and increased the level of interferon gamma (IFN-γ) in the plasma. In the tumor tissue, they caused an increase in the level of IL-10. Gene expression analysis of lung tissue demonstrated an increased level of osteopontin (Spp1) and transforming growth factor β (TGF-β) mRNA. The expression of Spp1 was also elevated in lymph nodes. Calcitriol and its analogs caused prevalence of tumor-conducive changes in the immune system of 4T1 tumor-bearing mice, despite the induction of some tumor-disadvantageous effects.

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