Eotaxin Augments Calcification in Vascular Smooth Muscle Cells

被引:13
作者
Raghuraman, Gayatri [1 ]
Hsiung, Joseph [1 ]
Zuniga, Mary C. [1 ]
Baughman, Brittanie D. [1 ]
Hitchner, Elizabeth [1 ]
Guzman, Raul J. [2 ]
Zhou, Wei [1 ,3 ]
机构
[1] VAPAHCS, Dept Vasc Surg, Palo Alto, CA USA
[2] Harvard Med Sch, Beth Israel Deaconess Hosp, Dept Surg, Boston, MA USA
[3] Stanford Univ, Dept Surg, Stanford, CA 94305 USA
关键词
EOTAXIN; OXIDATIVE STRESS; NADPH-OXIDASE; VASCULAR SMOOTH MUSCLE CELL; VASCULAR CALCIFICATION; OXIDATIVE STRESS; HUMAN ATHEROSCLEROSIS; POTENTIAL MECHANISM; INORGANIC-PHOSPHATE; ENDOTHELIAL-CELLS; BINDING PROTEIN; GENE-EXPRESSION; UP-REGULATION; IN-VIVO; DISEASE;
D O I
10.1002/jcb.25752
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Calcification of atherosclerotic plaques in elderly patients represents a potent risk marker of cardiovascular events. Plasma analyses of patients with or without calcified plaques reveal significant differences in chemokines, particularly eotaxin, which escalates with increased calcification. We therefore, hypothesize that eotaxin in circulation augments calcification of vascular smooth muscle cells (VSMCs) possibly via oxidative stress in the vasculature. We observe that eotaxin increases the rate of calcification significantly in VSMCs as evidenced by increased alkaline phosphatase activity, calcium deposition, and osteogenic marker expression. In addition, eotaxin promotes proliferation in VSMCs and triggers oxidative stress in a NADPH oxidase dependent manner. These primary novel observations support our proposition that in the vasculature eotaxin augments mineralization. Our findings suggest that eotaxin may represent a potential therapeutic target for prevention of cardiovascular complications in the elderly. J. Cell. Biochem. 118: 647-654, 2017. (c) 2016 Wiley Periodicals, Inc.
引用
收藏
页码:647 / 654
页数:8
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