IR@PKUHSC  > 北京大学基础医学院  > 生理学与病理生理学系
学科主题基础医学
Oxidant stress mechanism of homocysteine potentiating Con A-induced proliferation in murine splenic T lymphocytes
Zhang, Q; Zeng, XK; Guo, JX; Wang, M
关键词apoptosis atherosclerosis free radicals immunology infection/inflammation leukocytes
刊名CARDIOVASCULAR RESEARCH
2002-03-01
53期:4页:1035-1042
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Cardiac & Cardiovascular Systems
研究领域[WOS]Cardiovascular System & Cardiology
关键词[WOS]HUMAN ATHEROSCLEROTIC PLAQUES ; E-KNOCKOUT MICE ; SIGNAL-TRANSDUCTION ; HYDROGEN-PEROXIDE ; RISK FACTOR ; CELLS ; RECEPTOR ; GROWTH ; GENERATION ; ACTIVATION
英文摘要

Objective: An elevated plasma homocysteine (Hey) level is considered an independent risk factor for atherosclerosis. However, the mechanisms by which hyperhomocysteinemia induces atherosclerosis are only partially understood. The effect of Hey on T lymphocyte proliferation and its mechanisms were examined in normal and hyperhomocysteinemia ApoE-knockout mice. Methods: The mouse splenic T-cells were treated with Hey, related compounds and/or antioxidants in the presence or absence of Concanavalin A (Con A). DNA synthesis, cell apoptosis, interleukin-2 level and production of reactive oxygen species (ROS) were measured. Results: Hey (0.3-3.0 mM) and related compounds with thiol (-SH), such as cysteine and glutathione significantly potentiated Con A-induced proliferation and partially inhibited apoptosis in T lymphocytes, but it had no direct effect on resting T lymphocyte. ApoE-knockout mice with hyperhomocysteinemia (the level of plasma Hey was 20.3+/-2.9 vs. 2.6+/-0.6 muM in control group, P<0.05) had a significant promotion of T-cell proliferation in response to Con A. Hey (0.3-3.0 mM) also increased the intracellular ROS. Radical scavengers reduced Hey effect. Conclusions: These data indicate that ROS generated by thiol (-SH) of Hey auto-oxidation are involved in Hey effect on Con A-induced T lymphocyte proliferation. These findings suggest a novel mechanism may be involved in chronic inflammatory progression of atherosclerosis with hyperhomocysteinemia. (C) 2002 Elsevier Science BY All rights reserved.

语种英语
WOS记录号WOS:000175316800026
Citation statistics
Cited Times:37[WOS]   [WOS Record]     [Related Records in WOS]
文献类型期刊论文
版本出版稿
条目标识符http://ir.bjmu.edu.cn/handle/400002259/57119
Collection北京大学基础医学院_生理学与病理生理学系
作者单位1.Third Hosp, Inst Vasc Med, Beijing, Peoples R China
2.Peking Univ, Hlth Sci Ctr, Dept Physiol, Beijing 100083, Peoples R China
Recommended Citation
GB/T 7714
Zhang, Q,Zeng, XK,Guo, JX,et al. Oxidant stress mechanism of homocysteine potentiating Con A-induced proliferation in murine splenic T lymphocytes[J]. CARDIOVASCULAR RESEARCH,2002,53(4):1035-1042.
APA Zhang, Q,Zeng, XK,Guo, JX,&Wang, M.(2002).Oxidant stress mechanism of homocysteine potentiating Con A-induced proliferation in murine splenic T lymphocytes.CARDIOVASCULAR RESEARCH,53(4),1035-1042.
MLA Zhang, Q,et al."Oxidant stress mechanism of homocysteine potentiating Con A-induced proliferation in murine splenic T lymphocytes".CARDIOVASCULAR RESEARCH 53.4(2002):1035-1042.
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