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Fullerene Nanoparticles Selectively Enter Oxidation-Damaged Cerebral Microvessel Endothelial Cells and Inhibit JNK-Related Apoptosis
Lao, F; Chen, L; Li, W; Ge, CC; Qu, Y; Sun, QM; Zhao, YL; Han, D; Chen, CY; Zhao YL(赵宇亮)
2009
发表期刊ACS NANO
卷号3期号:11页码:3358-3368
通讯作者[Lao, Fang ; Chen, Long ; Qu, Ying ; Sun, Quanmei ; Han, Dong ; Chen, Chunying] Natl Ctr Nanosci & Technol NCNST, Beijing 100190, Peoples R China ; [Lao, Fang ; Chen, Long ; Li, Wei ; Ge, Cuicui ; Qu, Ying ; Sun, Quanmei ; Zhao, Yuliang ; Han, Dong ; Chen, Chunying] Chinese Acad Sci, NCNST, IHEP, Key Lab Biol Effects Nanomat & Nanosafety, Beijing 100049, Peoples R China
文章类型Article
摘要There is a dearth in fundamental cellular-level understanding of how nanoparticles interact with the cells of the blood brain barrier (BBB), particularly under the oxidative environment. The apoptosis of cerebral microvessel enclothelial cells (CMECs) induced by oxidative stress injury plays a key role in the dysfunction of BBB. By use of CMECs as an in vitro BBB model, we show for the first time that C(60)(C(COOH)(2))(2) nanoparticles can selectively enter oxidized CMECs rather than normal cells, and maintain CMECs integrity by attenuating H(2)O(2)-induced F-actin depolymerization via the observation of several state-of-the art microscopic techniques. Additionally, we have found that C(60)(C(COOH)(2))(2) nanoparticles greatly inhibit the apoptosis of CMECs induced by H(2)O(2), which is related to their modulation of the JNK pathway. C(60)(C(COOH)(2))(2) nanoparticles can regulate several downstream signaling events related to the JNK pathway, including reduction of JNK phosphorylation, activation of activator protein 1 (AP-1) and caspase-3, and inhibition of polyADP-ribose polymerase (PARP) cleavage and mitochondrial cytochrome c release. Our results indicate that C(60)(C(COOH)(2))(2) nanoparticles possess a novel ability of selectively entering oxidation-damaged cerebral enclothelial cells rather than normal enclothelial cells and then protecting them from apoptosis.
关键词C(60)(C(COOH)(2))(2) microvessel endothelial cells oxidative injury apoptosis JNK pathway
学科领域Chemistry; Science & Technology - Other Topics; Materials Science
研究领域[WOS]Chemistry ; Science & Technology - Other Topics ; Materials Science ; Chemistry ; Science & Technology - Other Topics ; Materials Science
DOI10.1021/nn900912n
URL查看原文
语种英语
研究领域[WOS]Chemistry ; Science & Technology - Other Topics ; Materials Science ; Chemistry ; Science & Technology - Other Topics ; Materials Science
WOS类目Chemistry, Multidisciplinary ; Chemistry, Physical ; Nanoscience & Nanotechnology ; Materials Science, Multidisciplinary
WOS记录号WOS:000271951200006
引用统计
被引频次:90[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/311005/239897
专题多学科研究中心
作者单位中国科学院高能物理研究所
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GB/T 7714
Lao, F,Chen, L,Li, W,et al. Fullerene Nanoparticles Selectively Enter Oxidation-Damaged Cerebral Microvessel Endothelial Cells and Inhibit JNK-Related Apoptosis[J]. ACS NANO,2009,3(11):3358-3368.
APA Lao, F.,Chen, L.,Li, W.,Ge, CC.,Qu, Y.,...&赵宇亮.(2009).Fullerene Nanoparticles Selectively Enter Oxidation-Damaged Cerebral Microvessel Endothelial Cells and Inhibit JNK-Related Apoptosis.ACS NANO,3(11),3358-3368.
MLA Lao, F,et al."Fullerene Nanoparticles Selectively Enter Oxidation-Damaged Cerebral Microvessel Endothelial Cells and Inhibit JNK-Related Apoptosis".ACS NANO 3.11(2009):3358-3368.
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