Endothelial-mesenchymal transition in atherosclerotic lesion calcification

被引：69

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

页码：124 / 127

页数：4

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