Administration of Additional Phosphorylated Prolactin During Pregnancy Inhibits Mammary Ductal Branching and Promotes Premature Lobuloalveolus Development

2001 ◽  
Author(s):  
Ameae M. Walker
Keyword(s):  
Ductal Branching ◽  
Phosphorylated Prolactin

scholarly journals Temporally regulated overexpression of parathyroid hormone-related protein in the mammary gland reveals distinct fetal and pubertal phenotypes

2001 ◽  
Vol 171 (3) ◽  
pp. 403-416 ◽  
Author(s):  
ME Dunbar ◽  
P Dann ◽  
CW Brown ◽  
J Van Houton ◽  
B Dreyer ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Parathyroid Hormone ◽  
Transgenic Mice ◽  
Mammary Development ◽  
Related Protein ◽  
Parathyroid Hormone Related Protein ◽  
Epithelial Cell Apoptosis ◽  
Ductal Elongation ◽  
Ductal Branching ◽  
Lobuloalveolar Development

We have previously demonstrated that overexpression of parathyroid hormone-related protein (PTHrP) in the mammary glands of transgenic mice results in defects in ductal elongation and branching during puberty and in lobuloalveolar development during pregnancy. In addition, we have shown that PTHrP is necessary for the formation of the initial ductal tree during embryonic mammary development. In order to examine the effect of varying the timing of PTHrP overexpression on mammary development, we created tetracycline-regulated, K14-tTA/Tet(O)-PTHrP double transgenic mice. In this report, we document that this 'tet-off' system directs transgene expression to the mammary gland and that it is fully repressed in the presence of tetracycline. Using these mice, we demonstrate that transient overexpression of PTHrP before birth causes defects in ductal branching during puberty and that overexpression of PTHrP during puberty decreases the rate of ductal elongation. Furthermore, we demonstrate that if PTHrP overexpression is initiated after ductal morphogenesis is completed, lobuloalveolar development is unaffected. Finally, we demonstrate that the impairment in ductal elongation caused by PTHrP is associated with an increase in the basal rate of epithelial cell apoptosis in terminal end buds and a failure to increase end bud cell proliferation and decrease apoptosis in response to estrogen and progesterone.

scholarly journals Stage-dependent regulation of mammary ductal branching by heparan sulfate and HGF-cMet signaling

2011 ◽  
Vol 355 (2) ◽  
pp. 394-403 ◽  
Author(s):  
Omai B. Garner ◽  
Kevin T. Bush ◽  
Kabir B. Nigam ◽  
Yu Yamaguchi ◽  
Ding Xu ◽  
...  
Keyword(s):  
Heparan Sulfate ◽  
Ductal Branching

Loss of CD24 expression promotes ductal branching in the murine mammary gland

2010 ◽  
Vol 67 (13) ◽  
pp. 2311-2322 ◽  
Author(s):  
Natascha Cremers ◽  
Marie-Ange Deugnier ◽  
Jonathan Sleeman
Keyword(s):  
Mammary Gland ◽  
Ductal Branching

scholarly journals Δn89β-Catenin Induces Precocious Development, Differentiation, and Neoplasia in Mammary Gland

2001 ◽  
Vol 153 (3) ◽  
pp. 555-568 ◽  
Author(s):  
Alexandra Imbert ◽  
Rachel Eelkema ◽  
Sara Jordan ◽  
Helen Feiner ◽  
Pamela Cowin
Keyword(s):  
Mammary Gland ◽  
Active Form ◽  
Mammary Glands ◽  
Downstream Effectors ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
Development And Differentiation ◽  
Pregnant Mice ◽  
Ductal Branching

To investigate the role of β-catenin in mammary gland development and neoplasia, we expressed a stabilized, transcriptionally active form of β-catenin lacking the NH2-terminal 89 amino acids (ΔN89β-catenin) under the control of the mouse mammary tumor virus long terminal repeat. Our results show that ΔN89β-catenin induces precocious lobuloalveolar development and differentiation in the mammary glands of both male and female mice. Virgin ΔN89β-catenin mammary glands resemble those found in wild-type (wt) pregnant mice and inappropriately express cyclin D1 mRNA. In contrast to wt mammary glands, which resume a virgin appearance after cessation of lactation, transgenic mammary glands involute to a midpregnant status. All transgenic females develop multiple aggressive adenocarcinomas early in life. Surprisingly, the ΔN89β-catenin phenotype differs from those elicited by overexpression of Wnt genes in this gland. In particular, ΔN89β-catenin has no effect on ductal side branching. This suggests that Wnt induction of ductal branching involves additional downstream effectors or modulators.

Opposite effects of unmodified prolactin and a molecular mimic of phosphorylated prolactin on morphology and the expression of prostate specific genes in the normal rat prostate

The Prostate ◽  
2002 ◽  
Vol 54 (1) ◽  
pp. 25-33 ◽  
Author(s):  
Xiaolei Xu ◽  
Wei Wu ◽  
Valencia Williams ◽  
Amy Khong ◽  
Yen-Hao Chen ◽  
...  
Keyword(s):  
Normal Rat ◽  
Rat Prostate ◽  
Phosphorylated Prolactin

Conditional loss of PTEN leads to precocious development and neoplasia in the mammary gland

Development ◽  
2002 ◽  
Vol 129 (17) ◽  
pp. 4159-4170 ◽  
Author(s):  
Gang Li ◽  
Gertraud W. Robinson ◽  
Ralf Lesche ◽  
Hilda Martinez-Diaz ◽  
Zhaorong Jiang ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Pten Gene ◽  
Mammary Tissue ◽  
Breast Cancers ◽  
Gene Mutant ◽  
Mammary Epithelia ◽  
Ductal Branching

PTEN tumor suppressor is frequently mutated in human cancers, including breast cancers. Female patients with inherited PTEN mutations suffer from virginal hypertrophy of the breast with high risk of malignant transformation. However, the exact mechanisms of PTEN in controlling mammary gland development and tumorigenesis are unclear. In this study, we generated mice with a mammary-specific deletion of the Pten gene. Mutant mammary tissue displayed precocious lobulo-alveolar development, excessive ductal branching, delayed involution and severely reduced apoptosis. Pten null mammary epithelial cells were disregulated and hyperproliferative. Mutant females developed mammary tumors early in life. Similar phenotypes were observed in Pten-null mammary epithelia that had been transplanted into wild-type stroma, suggesting that PTEN plays an essential and cell-autonomous role in controlling the proliferation, differentiation and apoptosis of mammary epithelial cells.

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