scholarly journals Ltbp1Lis focally induced in embryonic mammary mesenchyme, demarcates the ductal luminal lineage and is upregulated during involution

2013 ◽  
Vol 15 (6) ◽  
Author(s):  
Anupama Chandramouli ◽  
Julia Simundza ◽  
Alicia Pinderhughes ◽  
Minoti Hiremath ◽  
Gustavo Droguett ◽  
...  
Keyword(s):  
Mammary Mesenchyme

Parathyroid hormone-related protein maintains mammary epithelial fate and triggers nipple skin differentiation during embryonic breast development

Development ◽  
2001 ◽  
Vol 128 (4) ◽  
pp. 513-525 ◽  
Author(s):  
J. Foley ◽  
P. Dann ◽  
J. Hong ◽  
J. Cosgrove ◽  
B. Dreyer ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Epithelial Cells ◽  
Cell Fate ◽  
Mesenchymal Cells ◽  
Mammary Development ◽  
Mammary Epithelial ◽  
Related Protein ◽  
Parathyroid Hormone Related Protein ◽  
Mammary Mesenchyme ◽  
Pthrp Receptor

Prior reports have demonstrated that both parathyroid hormone-related protein (PTHrP) and the type I PTH/PTHrP receptor are necessary for the proper development of the embryonic mammary gland in mice. Using a combination of loss-of-function and gain-of-function models, we now report that PTHrP regulates a series of cell fate decisions that are central to the survival and morphogenesis of the mammary epithelium and the formation of the nipple. PTHrP is made in the epithelial cells of the mammary bud and, during embryonic mammary development, it interacts with the surrounding mesenchymal cells to induce the formation of the dense mammary mesenchyme. In response, these mammary-specific mesenchymal cells support the maintenance of mammary epithelial cell fate, trigger epithelial morphogenesis and induce the overlying epidermis to form the nipple. In the absence of PTHrP signaling, the mammary epithelial cells revert to an epidermal fate, no mammary ducts are formed and the nipple does not form. In the presence of diffuse epidermal PTHrP signaling, the ventral dermis is transformed into mammary mesenchyme and the entire ventral epidermis becomes nipple skin. These alterations in cell fate require that PTHrP be expressed during development and they require the presence of the PTH/PTHrP receptor. Finally, PTHrP signaling regulates the epidermal and mesenchymal expression of LEF1 and (β)-catenin, suggesting that these changes in cell fate involve an interaction between the PTHrP and Wnt signaling pathways.

scholarly journals Parathyroid hormone-related protein activates Wnt signaling to specify the embryonic mammary mesenchyme

Development ◽  
2012 ◽  
Vol 139 (22) ◽  
pp. 4239-4249 ◽  
Author(s):  
M. Hiremath ◽  
P. Dann ◽  
J. Fischer ◽  
D. Butterworth ◽  
K. Boras-Granic ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Wnt Signaling ◽  
Related Protein ◽  
Parathyroid Hormone Related Protein ◽  
Mammary Mesenchyme

Mammary Phenotypic Expression Induced in Epidermal Cells by Embryonic Mammary Mesenchyme

1995 ◽  
Vol 152 (3) ◽  
pp. 195-204 ◽  
Author(s):  
GR. Cunha ◽  
P. Young ◽  
K. Christov ◽  
R. Guzman ◽  
S. Nandi ◽  
...  
Keyword(s):  
Phenotypic Expression ◽  
Epidermal Cells ◽  
Mammary Mesenchyme

Parathyroid hormone-related protein signaling is necessary for sexual dimorphism during embryonic mammary development

Development ◽  
1999 ◽  
Vol 126 (16) ◽  
pp. 3485-3493
Author(s):  
M.E. Dunbar ◽  
P.R. Dann ◽  
G.W. Robinson ◽  
L. Hennighausen ◽  
J.P. Zhang ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Cell Fate ◽  
Ectopic Expression ◽  
Mammary Development ◽  
Mammary Epithelial ◽  
Related Protein ◽  
Cell Fate Decisions ◽  
Parathyroid Hormone Related Protein ◽  
Pthrp Expression ◽  
Mammary Mesenchyme

Male mice lack mammary glands due to the interaction of circulating androgens with local epithelial-mesenchymal signaling in the developing mammary bud. Mammary epithelial cells induce androgen receptor (AR) within the mammary mesenchyme and, in response to androgens, the mesenchyme condenses around the epithelial bud, destroying it. We show that this process involves apoptosis and that, in the absence of parathyroid hormone-related protein (PTHrP) or its receptor, the PTH/PTHrP receptor (PPR1), it fails due to a lack of mesenchymal AR expression. In addition, the expression of tenascin C, another marker of the mammary mesenchyme, is also dependent on PTHrP. PTHrP expression is initiated on E11 and, within the ventral epidermis, is restricted to the forming mammary epithelial bud. In contrast, PPR1 expression is not limited to the mammary bud, but is found generally within the subepidermal mesenchyme. Finally, transgenic overexpression of PTHrP within the basal epidermis induces AR and tenasin C expression within the ventral dermis, suggesting that ectopic expression of PTHrP can induce the ventral mesenchyme to express mammary mesenchyme markers. We propose that PTHrP expression specifically within the developing epithelial bud acts as a dominant signal participating in cell fate decisions leading to a specialized mammary mesenchyme.

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