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