Endothelial-mesenchymal transition in vascular calcification of Ins2Akita/+ Mice

Pierre J. Guihard; Jiayi Yao; Ana M. Blazquez-Medela; Luisa Iruela-Arispe; Kristina I. Boström; Yucheng Yao

doi:10.1371/journal.pone.0167936

Endothelial-mesenchymal transition in vascular calcification of Ins2Akita/+ Mice

Pierre J. Guihard, Jiayi Yao, Ana M. Blazquez-Medela, Luisa Iruela-Arispe, Kristina I. Boström, Yucheng Yao

Cell & Developmental Biology

Research output: Contribution to journal › Article › peer-review

24 Scopus citations

Abstract

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 Ins2Akita/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.

Original language	English (US)
Article number	e0167936
Journal	PloS one
Volume	11
Issue number	12
DOIs	https://doi.org/10.1371/journal.pone.0167936
State	Published - Dec 2016

Funding

Funding for this work was provided in part by NIH grants NS79353, HL30568, HL81397 and HL112839, and the American Heart Association (Western Affiliate).

ASJC Scopus subject areas

General

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1371/journal.pone.0167936

Cite this

@article{41c3d256be3048a6b84e2ee77a59059d,

title = "Endothelial-mesenchymal transition in vascular calcification of Ins2Akita/+ Mice",

abstract = "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 Ins2Akita/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.",

author = "Guihard, {Pierre J.} and Jiayi Yao and Blazquez-Medela, {Ana M.} and Luisa Iruela-Arispe and Bostr{\"o}m, {Kristina I.} and Yucheng Yao",

note = "Publisher Copyright: {\textcopyright} 2016 Guihard et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.",

year = "2016",

month = dec,

doi = "10.1371/journal.pone.0167936",

language = "English (US)",

volume = "11",

journal = "PloS one",

issn = "1932-6203",

publisher = "Public Library of Science",

number = "12",

}

TY - JOUR

T1 - Endothelial-mesenchymal transition in vascular calcification of Ins2Akita/+ Mice

AU - Guihard, Pierre J.

AU - Yao, Jiayi

AU - Blazquez-Medela, Ana M.

AU - Iruela-Arispe, Luisa

AU - Boström, Kristina I.

AU - Yao, Yucheng

N1 - Publisher Copyright: © 2016 Guihard et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

PY - 2016/12

Y1 - 2016/12

N2 - 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 Ins2Akita/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.

AB - 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 Ins2Akita/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.

UR - http://www.scopus.com/inward/record.url?scp=85005967103&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85005967103&partnerID=8YFLogxK

U2 - 10.1371/journal.pone.0167936

DO - 10.1371/journal.pone.0167936

M3 - Article

C2 - 27936229

AN - SCOPUS:85005967103

SN - 1932-6203

VL - 11

JO - PloS one

JF - PloS one

IS - 12

M1 - e0167936

ER -

Endothelial-mesenchymal transition in vascular calcification of Ins2Akita/+ Mice

Abstract

Funding

ASJC Scopus subject areas

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this