Precocious Mammary Gland Development in P-Cadherin–deficient Mice
To investigate the functions of P-cadherin in vivo, we have mutated the gene encoding this cell adhesion receptor in mice. In contrast to E- and N-cadherin– deficient mice, mice homozygous for the P-cadherin mutation are viable. Although P-cadherin is expressed at high levels in the placenta, P-cadh...
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| Format: | Online |
| Language: | English |
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The Rockefeller University Press
1997
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| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2139972/ |
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pubmed-21399722008-05-01 Precocious Mammary Gland Development in P-Cadherin–deficient Mice Radice, Glenn L. Ferreira-Cornwell, M. Celeste Robinson, Stephen D. Rayburn, Helen Chodosh, Lewis A. Takeichi, Masatoshi Hynes, Richard O. Article To investigate the functions of P-cadherin in vivo, we have mutated the gene encoding this cell adhesion receptor in mice. In contrast to E- and N-cadherin– deficient mice, mice homozygous for the P-cadherin mutation are viable. Although P-cadherin is expressed at high levels in the placenta, P-cadherin–null females are fertile. P-cadherin expression is localized to the myoepithelial cells surrounding the lumenal epithelial cells of the mammary gland. The role of the myoepithelium as a contractile tissue necessary for milk secretion is clear, but its function in the nonpregnant animal is unknown. The ability of the P-cadherin mutant female to nurse and maintain her litter indicates that the contractile function of the myoepithelium is not dependent on the cell adhesion molecule P-cadherin. The virgin P-cadherin–null females display precocious differentiation of the mammary gland. The alveolar-like buds in virgins resemble the glands of an early pregnant animal morphologically and biochemically (i.e., milk protein synthesis). The P-cadherin mutant mice develop hyperplasia and dysplasia of the mammary epithelium with age. In addition, abnormal lymphocyte infiltration was observed in the mammary glands of the mutant animals. These results indicate that P-cadherin–mediated adhesion and/or signals derived from cell–cell interactions are important determinants in negative growth control in the mammary gland. Furthermore, the loss of P-cadherin from the myoepithelium has uncovered a novel function for this tissue in maintaining the undifferentiated state of the underlying secretory epithelium. The Rockefeller University Press 1997-11-17 /pmc/articles/PMC2139972/ /pubmed/9362520 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
| repository_type |
Open Access Journal |
| institution_category |
Foreign Institution |
| institution |
US National Center for Biotechnology Information |
| building |
NCBI PubMed |
| collection |
Online Access |
| language |
English |
| format |
Online |
| author |
Radice, Glenn L. Ferreira-Cornwell, M. Celeste Robinson, Stephen D. Rayburn, Helen Chodosh, Lewis A. Takeichi, Masatoshi Hynes, Richard O. |
| spellingShingle |
Radice, Glenn L. Ferreira-Cornwell, M. Celeste Robinson, Stephen D. Rayburn, Helen Chodosh, Lewis A. Takeichi, Masatoshi Hynes, Richard O. Precocious Mammary Gland Development in P-Cadherin–deficient Mice |
| author_facet |
Radice, Glenn L. Ferreira-Cornwell, M. Celeste Robinson, Stephen D. Rayburn, Helen Chodosh, Lewis A. Takeichi, Masatoshi Hynes, Richard O. |
| author_sort |
Radice, Glenn L. |
| title |
Precocious Mammary Gland Development in P-Cadherin–deficient Mice |
| title_short |
Precocious Mammary Gland Development in P-Cadherin–deficient Mice |
| title_full |
Precocious Mammary Gland Development in P-Cadherin–deficient Mice |
| title_fullStr |
Precocious Mammary Gland Development in P-Cadherin–deficient Mice |
| title_full_unstemmed |
Precocious Mammary Gland Development in P-Cadherin–deficient Mice |
| title_sort |
precocious mammary gland development in p-cadherin–deficient mice |
| description |
To investigate the functions of P-cadherin in vivo, we have mutated the gene encoding this cell adhesion receptor in mice. In contrast to E- and N-cadherin– deficient mice, mice homozygous for the P-cadherin mutation are viable. Although P-cadherin is expressed at high levels in the placenta, P-cadherin–null females are fertile. P-cadherin expression is localized to the myoepithelial cells surrounding the lumenal epithelial cells of the mammary gland. The role of the myoepithelium as a contractile tissue necessary for milk secretion is clear, but its function in the nonpregnant animal is unknown. The ability of the P-cadherin mutant female to nurse and maintain her litter indicates that the contractile function of the myoepithelium is not dependent on the cell adhesion molecule P-cadherin. The virgin P-cadherin–null females display precocious differentiation of the mammary gland. The alveolar-like buds in virgins resemble the glands of an early pregnant animal morphologically and biochemically (i.e., milk protein synthesis). The P-cadherin mutant mice develop hyperplasia and dysplasia of the mammary epithelium with age. In addition, abnormal lymphocyte infiltration was observed in the mammary glands of the mutant animals. These results indicate that P-cadherin–mediated adhesion and/or signals derived from cell–cell interactions are important determinants in negative growth control in the mammary gland. Furthermore, the loss of P-cadherin from the myoepithelium has uncovered a novel function for this tissue in maintaining the undifferentiated state of the underlying secretory epithelium. |
| publisher |
The Rockefeller University Press |
| publishDate |
1997 |
| url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2139972/ |
| _version_ |
1611422036836483072 |