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Endothelial dysfunction and inflammation induced by iron oxide nanoparticle exposure: Risk factors for early atherosclerosis
Zhu MT(朱墨桃); Wang B(汪冰); Wang Y(王云); Wang HJ(王华建); Wang M(王萌); Ou YH(欧阳宏); Chai ZF(柴之芳); Feng WY(丰伟悦); Zhao YL(赵宇亮); Zhu, MT; Wang, B; Wang, Y; Yuan, L; Wang, HJ; Wang, M; Ouyang, H; Chai, ZF; Feng, WY; Zhao, YL
2011
发表期刊TOXICOLOGY LETTERS
卷号203期号:2页码:#REF!
通讯作者Feng, WY (reprint author), Chinese Acad Sci, Inst High Energy Phys, CAS Key Lab Biomed Effects Nanomat & Nanosafety, POB 918, Beijing 100049, Peoples R China.
文章类型Article
摘要More recently, the correlation between exposure to nanoparticles and cardiovascular diseases is of particular concern in nanotoxicology related fields. Nanoparticle-triggered endothelial dysfunction is hypothesized to be a dominant mechanism in the development of the diseases. To test this hypothesis. iron oxide nanoparticles (Fe(2)O(3) and Fe(3)O(4)), as two widely used nanomaterials and the main metallic components in particulate matter, were selected to assess their potential risks on human endothelial system. The direct effects of iron oxide nanoparticles on human aortic endothelial cells (HAECs) and the possible effects mediated by monocyte (U937 cells) phagocytosis and activation were investigated. In the study, HAECs and U937 cells were exposed to 2, 20, 100 mu g/mL of 22-nm-Fe(2)O(3) and 43-nm-Fe(3)O(4) particles. Our results indicate that cytoplasmic vacuolation, mitochondrial swelling and cell death were induced in HAEC. A significant increase in nitric oxide (NO) production was induced which coincided with the elevation of nitric oxide synthase (NOS) activity in HAECs. Adhesion of monocytes to the HAECs was significantly enhanced as a consequence of the up-regulation of intracellular cell adhesion molecule-1 (ICAM-1) and interleukin-8 (IL-8) expression, all of which are considered as early steps of atheroscelerosis. Phagocytosis and dissolution of nanoparticles by monocytes were found to simultaneously provoke oxidative stress and mediate severe endothelial toxicity. We conclude that intravascular iron oxide nanoparticles may induce endothelial system inflammation and dysfunction by three ways: (1) nanoparticles may escape from phagocytosis that interact directly with the endothelial monolayer; (2) nanoparticles are phagocytized by monocytes and then dissolved, thus impact the endothelial cells as free iron ions; or (3) nanoparticles are phagocytized by monocytes to provoke oxidative stress responses. (C) 2011 Published by Elsevier Ireland Ltd.
关键词Iron oxide nanoparticle Human aortic endothelial cells Atheroscelerosis Endothelial dysfunction Human monocyte
学科领域Toxicology
DOI10.1016/j.toxlet.2011.03.021
收录类别SCI
WOS类目Toxicology
WOS记录号WOS:000291140400010
引用统计
被引频次:117[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.ihep.ac.cn/handle/311005/226603
专题院士
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GB/T 7714
Zhu MT,Wang B,Wang Y,et al. Endothelial dysfunction and inflammation induced by iron oxide nanoparticle exposure: Risk factors for early atherosclerosis[J]. TOXICOLOGY LETTERS,2011,203(2):#REF!.
APA 朱墨桃.,汪冰.,王云.,王华建.,王萌.,...&Zhao, YL.(2011).Endothelial dysfunction and inflammation induced by iron oxide nanoparticle exposure: Risk factors for early atherosclerosis.TOXICOLOGY LETTERS,203(2),#REF!.
MLA 朱墨桃,et al."Endothelial dysfunction and inflammation induced by iron oxide nanoparticle exposure: Risk factors for early atherosclerosis".TOXICOLOGY LETTERS 203.2(2011):#REF!.
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