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Endothelial-Mesenchymal Transition in Vascular Calcification of Ins2(Akita/+) Mice
Endothelial-mesenchymal transition (EndMT) drives endothelium to contribute to normal development and disease processes. Here, we report that EndMTs occur in the diabetic endothelium of Ins2(Akita/wt) mouse, and show that induction of sex determining region Y-box 2 (Sox2) is a mediator of excess BMP...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5148029/ https://www.ncbi.nlm.nih.gov/pubmed/27936229 http://dx.doi.org/10.1371/journal.pone.0167936 |
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author | Guihard, Pierre J. Yao, Jiayi Blazquez-Medela, Ana M. Iruela-Arispe, Luisa Boström, Kristina I. Yao, Yucheng |
author_facet | Guihard, Pierre J. Yao, Jiayi Blazquez-Medela, Ana M. Iruela-Arispe, Luisa Boström, Kristina I. Yao, Yucheng |
author_sort | Guihard, Pierre J. |
collection | PubMed |
description | Endothelial-mesenchymal transition (EndMT) drives endothelium to contribute to normal development and disease processes. Here, we report that EndMTs occur in the diabetic endothelium of Ins2(Akita/wt) mouse, and show that induction of sex determining region Y-box 2 (Sox2) is a mediator of excess BMP signaling that results in activation of EndMTs and increased vascular calcification. We also find an induction of a complex of serine proteases in the diabetic endothelium, required for the up-regulation of Sox2. Our results suggest that EndMTs contribute to vascular calcification in diabetic arteries. |
format | Online Article Text |
id | pubmed-5148029 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-51480292016-12-28 Endothelial-Mesenchymal Transition in Vascular Calcification of Ins2(Akita/+) Mice Guihard, Pierre J. Yao, Jiayi Blazquez-Medela, Ana M. Iruela-Arispe, Luisa Boström, Kristina I. Yao, Yucheng PLoS One Research Article Endothelial-mesenchymal transition (EndMT) drives endothelium to contribute to normal development and disease processes. Here, we report that EndMTs occur in the diabetic endothelium of Ins2(Akita/wt) mouse, and show that induction of sex determining region Y-box 2 (Sox2) is a mediator of excess BMP signaling that results in activation of EndMTs and increased vascular calcification. We also find an induction of a complex of serine proteases in the diabetic endothelium, required for the up-regulation of Sox2. Our results suggest that EndMTs contribute to vascular calcification in diabetic arteries. Public Library of Science 2016-12-09 /pmc/articles/PMC5148029/ /pubmed/27936229 http://dx.doi.org/10.1371/journal.pone.0167936 Text en © 2016 Guihard 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 Guihard, Pierre J. Yao, Jiayi Blazquez-Medela, Ana M. Iruela-Arispe, Luisa Boström, Kristina I. Yao, Yucheng Endothelial-Mesenchymal Transition in Vascular Calcification of Ins2(Akita/+) Mice |
title | Endothelial-Mesenchymal Transition in Vascular Calcification of Ins2(Akita/+) Mice |
title_full | Endothelial-Mesenchymal Transition in Vascular Calcification of Ins2(Akita/+) Mice |
title_fullStr | Endothelial-Mesenchymal Transition in Vascular Calcification of Ins2(Akita/+) Mice |
title_full_unstemmed | Endothelial-Mesenchymal Transition in Vascular Calcification of Ins2(Akita/+) Mice |
title_short | Endothelial-Mesenchymal Transition in Vascular Calcification of Ins2(Akita/+) Mice |
title_sort | endothelial-mesenchymal transition in vascular calcification of ins2(akita/+) mice |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5148029/ https://www.ncbi.nlm.nih.gov/pubmed/27936229 http://dx.doi.org/10.1371/journal.pone.0167936 |
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