Mid‐region parathyroid hormone‐related protein is a genome‐wide chromatin‐binding factor that promotes growth and differentiation of HB2 epithelial cells from the human breast

BioFactors ◽  
2018 ◽  
Vol 45 (2) ◽  
pp. 279-288 ◽  
Author(s):  
Claudio Luparello ◽  
Mariangela Librizzi ◽  
Dalia M. L. Asaro ◽  
Ilenia Cruciata ◽  
Fabio Caradonna
Keyword(s):  
Parathyroid Hormone ◽  
Epithelial Cells ◽  
Chromatin Binding ◽  
Related Protein ◽  
Human Breast ◽  
Parathyroid Hormone Related Protein ◽  
Genome Wide ◽  
A Genome ◽  
Binding Factor

Ets-1 activates parathyroid hormone-related protein gene expression in tumorigenic breast epithelial cells

2003 ◽  
Vol 204 (1-2) ◽  
pp. 155-168 ◽  
Author(s):  
Christophe Cataisson ◽  
Johnthan Gordon ◽  
Mickael Roussière ◽  
Arman Abdalkhani ◽  
Ralph Lindemannn ◽  
...  
Keyword(s):  
Gene Expression ◽  
Parathyroid Hormone ◽  
Epithelial Cells ◽  
Protein Gene ◽  
Related Protein ◽  
Breast Epithelial Cells ◽  
Parathyroid Hormone Related Protein ◽  
Breast Epithelial

Parathyroid hormone-related protein increases cAMP production in mammary epithelial cells

1993 ◽  
Vol 264 (3) ◽  
pp. E471-E475 ◽  
Author(s):  
S. Ferrari ◽  
R. Rizzoli ◽  
C. Chaponnier ◽  
G. Gabbiani ◽  
J. P. Bonjour
Keyword(s):  
Parathyroid Hormone ◽  
Epithelial Cells ◽  
Breast Tissue ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Immunofluorescent Staining ◽  
Regulatory Function ◽  
Related Protein ◽  
Camp Production ◽  
Parathyroid Hormone Related Protein

Parathyroid hormone-related protein (PTHrP) is a major cause of malignant hypercalcemia but has been found in many nontumoral tissues as well. Thus it is produced by the mammary gland during lactation and released into milk. Whether PTHrP directly affects breast tissue is however not known. We investigated the effects of PTHrP on adenosine 3',5'-cyclic monophosphate (cAMP) production in primary cultures of mammary epithelial cells isolated from lactating rats. On the 7th day in culture, synthetic PTHrP-(1-34), recombinant (r) PTHrP-(1-108), and rPTHrP-(1-141) stimulated cAMP production in a concentration-dependent manner. Thus PTHrP-(1-34) induced a 1.92 +/- 0.04-fold stimulation of cAMP production (mean +/- SE, n = 5 separate experiments, P < 0.001). At the time of maximal responsiveness to PTHrP, a significant proportion of the cells was characterized by an elongated shape and a positive immunofluorescent staining for both prekeratin and alpha-smooth muscle actin 1, compatible with a myoepithelial phenotype. It therefore appears that PTHrP can stimulate the production of cAMP in mammary cells, suggesting a possible autocrine/paracrine regulatory function for PTHrP in breast tissue.

Cortisol, parathyroid hormone-related protein and the onset of calcium secretion by the mammary gland of the goat

1997 ◽  
Vol 64 (4) ◽  
pp. 633-636
Author(s):  
GORDON E. THOMPSON ◽  
S. KHAWAR ABBAS ◽  
CARL HOLT ◽  
ANTHONY D. CARE
Keyword(s):  
Mammary Gland ◽  
Parathyroid Hormone ◽  
Epithelial Cells ◽  
Tight Junctions ◽  
Calcium Transport ◽  
Extracellular Fluid ◽  
Secretory Cells ◽  
Related Protein ◽  
Parathyroid Hormone Related Protein ◽  
Calcium Secretion

During lactogenesis in the goat, the onset of secretion of calcium into milk occurs at parturition (Thompson et al. 1995) at approximately the same time as the onset of secretion of parathyroid hormone-related protein (PTHrP) by the mammary gland (Ratcliffe et al. 1992); these events may be unrelated or PTHrP may be involved in calcium transport from blood to milk.Parturition in goats is initiated by fetal secretion of cortisol (Flint et al. 1978) and maternal secretion of cortisol also increases (Paterson & Linzell, 1971). Injecting cortisol locally into the sinus of a mammary gland of the late-pregnant goat when the tight junctions between secretory epithelial cells appear to be ‘loose’, and injectate can reach the basolateral surfaces of secretory cells, stimulates an early tightening of these junctions (Thompson, 1996) as occurs naturally at parturition. This tightening can be produced by an increased concentration of ionized calcium in the extracellular fluid of the gland (Neville & Peaker, 1981).The experiments reported here were undertaken to determine if cortisol injection stimulates the mammary gland to secrete both PTHrP and calcium before parturition.

The expression of parathyroid hormone-related protein in human breast cancer with skeletal metastases

Surgery Today ◽  
1994 ◽  
Vol 24 (3) ◽  
pp. 215-220 ◽  
Author(s):  
Norio Kohno ◽  
Sohei Kitazawa ◽  
Masaaki Fukase ◽  
Yoko Sakoda ◽  
Yoshihiro Kanbara ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Parathyroid Hormone ◽  
Human Breast Cancer ◽  
Skeletal Metastases ◽  
Related Protein ◽  
Human Breast ◽  
Parathyroid Hormone Related Protein

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.

Sign in / Sign up

Export Citation Format

Share Document