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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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Autores principales: Radice, Glenn L., Ferreira-Cornwell, M. Celeste, Robinson, Stephen D., Rayburn, Helen, Chodosh, Lewis A., Takeichi, Masatoshi, Hynes, Richard O.
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1997
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2139972/
https://www.ncbi.nlm.nih.gov/pubmed/9362520
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author Radice, Glenn L.
Ferreira-Cornwell, M. Celeste
Robinson, Stephen D.
Rayburn, Helen
Chodosh, Lewis A.
Takeichi, Masatoshi
Hynes, Richard O.
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.
collection PubMed
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.
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spelling 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. J Cell Biol 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/).
spellingShingle Article
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
title 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_short Precocious Mammary Gland Development in P-Cadherin–deficient Mice
title_sort precocious mammary gland development in p-cadherin–deficient mice
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2139972/
https://www.ncbi.nlm.nih.gov/pubmed/9362520
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