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Loss of caveolin-1 alters extracellular matrix protein expression and ductal architecture in murine mammary glands

The extracellular matrix (ECM) is abnormal in breast tumors and has been reported to contribute to breast tumor progression. One factor, which may drive ongoing matrix synthesis in breast tumors, is the loss of stromal caveolin-1 (cav-1), a scaffolding protein of caveolae, which has been linked to b...

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Autores principales: Thompson, Christopher, Rahim, Sahar, Arnold, Jeremiah, Hielscher, Abigail
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5302825/
https://www.ncbi.nlm.nih.gov/pubmed/28187162
http://dx.doi.org/10.1371/journal.pone.0172067
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author Thompson, Christopher
Rahim, Sahar
Arnold, Jeremiah
Hielscher, Abigail
author_facet Thompson, Christopher
Rahim, Sahar
Arnold, Jeremiah
Hielscher, Abigail
author_sort Thompson, Christopher
collection PubMed
description The extracellular matrix (ECM) is abnormal in breast tumors and has been reported to contribute to breast tumor progression. One factor, which may drive ongoing matrix synthesis in breast tumors, is the loss of stromal caveolin-1 (cav-1), a scaffolding protein of caveolae, which has been linked to breast tumor aggressiveness. To determine whether loss of cav-1 results in the abnormal expression of matrix proteins, mammary glands from cav- 1-/- and cav- 1 +/+ mice were investigated for differences in expression of several ECM proteins. In addition, the presence of myofibroblasts, changes in the vessel density, and differences in duct number and size were assessed in the mammary glands of both animal models. Using immunohistochemistry, expression of fibronectin, tenascin-C, collagens and αSMA were significantly increased in the mammary glands of cav-1-/- mice. Second harmonic generation revealed more organized collagen fibers in cav-1 -/- glands and supported immunohistochemical analyses of increased collagen abundance in the glands of cav-1 -/- mice. Analysis of the ductal structure demonstrated a significant increase in the number of proliferating ducts in addition to significant increases in the duct circumference and area in cav-1 -/- glands compared to cav- 1 +/+ glands. Differences in microvessel density weren’t apparent between the animal models. In summary, we found that the loss of cav-1 resulted in increased ECM and α-SMA protein expression in murine mammary glands. Furthermore, we found that an abnormal ductal architecture accompanied the loss of cav-1. These data support a role for cav-1 in maintaining mammary gland structure.
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spelling pubmed-53028252017-02-28 Loss of caveolin-1 alters extracellular matrix protein expression and ductal architecture in murine mammary glands Thompson, Christopher Rahim, Sahar Arnold, Jeremiah Hielscher, Abigail PLoS One Research Article The extracellular matrix (ECM) is abnormal in breast tumors and has been reported to contribute to breast tumor progression. One factor, which may drive ongoing matrix synthesis in breast tumors, is the loss of stromal caveolin-1 (cav-1), a scaffolding protein of caveolae, which has been linked to breast tumor aggressiveness. To determine whether loss of cav-1 results in the abnormal expression of matrix proteins, mammary glands from cav- 1-/- and cav- 1 +/+ mice were investigated for differences in expression of several ECM proteins. In addition, the presence of myofibroblasts, changes in the vessel density, and differences in duct number and size were assessed in the mammary glands of both animal models. Using immunohistochemistry, expression of fibronectin, tenascin-C, collagens and αSMA were significantly increased in the mammary glands of cav-1-/- mice. Second harmonic generation revealed more organized collagen fibers in cav-1 -/- glands and supported immunohistochemical analyses of increased collagen abundance in the glands of cav-1 -/- mice. Analysis of the ductal structure demonstrated a significant increase in the number of proliferating ducts in addition to significant increases in the duct circumference and area in cav-1 -/- glands compared to cav- 1 +/+ glands. Differences in microvessel density weren’t apparent between the animal models. In summary, we found that the loss of cav-1 resulted in increased ECM and α-SMA protein expression in murine mammary glands. Furthermore, we found that an abnormal ductal architecture accompanied the loss of cav-1. These data support a role for cav-1 in maintaining mammary gland structure. Public Library of Science 2017-02-10 /pmc/articles/PMC5302825/ /pubmed/28187162 http://dx.doi.org/10.1371/journal.pone.0172067 Text en © 2017 Thompson et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Thompson, Christopher
Rahim, Sahar
Arnold, Jeremiah
Hielscher, Abigail
Loss of caveolin-1 alters extracellular matrix protein expression and ductal architecture in murine mammary glands
title Loss of caveolin-1 alters extracellular matrix protein expression and ductal architecture in murine mammary glands
title_full Loss of caveolin-1 alters extracellular matrix protein expression and ductal architecture in murine mammary glands
title_fullStr Loss of caveolin-1 alters extracellular matrix protein expression and ductal architecture in murine mammary glands
title_full_unstemmed Loss of caveolin-1 alters extracellular matrix protein expression and ductal architecture in murine mammary glands
title_short Loss of caveolin-1 alters extracellular matrix protein expression and ductal architecture in murine mammary glands
title_sort loss of caveolin-1 alters extracellular matrix protein expression and ductal architecture in murine mammary glands
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5302825/
https://www.ncbi.nlm.nih.gov/pubmed/28187162
http://dx.doi.org/10.1371/journal.pone.0172067
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