Endothelial-mesenchymal transition in atherosclerotic lesion calcification

被引：66
|
作者：
Bostroem, Kristina I. [1 ,2 ]
Yao, Jiayi [1 ]
Guihard, Pierre J. [1 ]
Blazquez-Medela, Ana M. [1 ]
Yao, Yucheng [1 ,3 ]
机构：
[1] Univ Calif Los Angeles, David Geffen Sch Med, Div Cardiol, Los Angeles, CA 90095 USA
[2] Univ Calif Los Angeles, Inst Mol Biol, Los Angeles, CA 90095 USA
[3] Univ Calif Los Angeles, Johnsson Comprehens Canc Ctr, Los Angeles, CA 90095 USA
来源：
ATHEROSCLEROSIS | 2016年 / 253卷
关键词：
Endothelial-mesenchymal transition; Atherosclerotic lesion calcification; Sex-determining region Y-box 2; Serine protease; Endothelial cells; REGULATORY MECHANISMS; VASCULAR-DISEASE; INHIBITION;
D O I：
10.1016/j.atherosclerosis.2016.08.046
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
Background and aims: Endothelial-mesenchymal transitions (EndMTs) in endothelial cells (ECs) contribute to vascular disease. Methods: We used ApoE(-/-) mice fed a high-fat/high-cholesterol diet. Results: We reported evidence of EndMT in atherosclerotic lesions contributing to calcification. Stem cell and mesenchymal markers, including sex-determining region Y-box 2 (Sox2), were upregulated in aortic ECs of fat-fed ApoE(-/-) mice. Limiting Sox2 decreased marker expression and calcification in ApoE(-/-) aortas. Furthermore, a complex of serine proteases was upregulated in ApoE(-/-) aortic ECs. Blockade of these proteases reduced expression of Sox2 and atherosclerotic lesion calcification. Conclusions: Together, our data suggest that EndMTs contribute to atherosclerotic lesion calcification. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码：124 / 127
页数：4
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