High-density lipoprotein inhibits migration of vascular smooth muscle cells through its sphingosine 1-phosphate component
High-density lipoprotein inhibits migration of vascular smooth muscle cells through its sphingosine 1-phosphate component
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DOI：
10.1016/j.atherosclerosis.2004.07.032
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发表时间：
2005-01-01
期刊：
影响因子：
5.3
通讯作者：
Okajima, F
中科院分区：
文献类型：
--
作者：
Tamama, K;Tomura, H;Okajima, F
高密度脂蛋白(高密度脂蛋白)是一种公认的抗动脉粥样硬化风险因子。但其抗动脉粥样硬化作用的机制尚不完全清楚。在这里，我们研究了高密度脂蛋白相关的鞘氨醇I-磷酸(SIP)的作用。一个Lysolipid调解人。在脂蛋白诱导的大鼠血管平滑肌细胞(VSMCs)中的作用。高密度脂蛋白和苏糖核酸均可抑制血小板衍生生长因子诱导的VSMC迁移。这种抑制作用与抑制细胞扩散有关，这些反应是。用SIP使VSMC脱敏而逆转。高密度脂蛋白和大豆多糖核酸对中国仓鼠卵巢细胞的迁移也有抑制作用，这种作用可通过过度表达SIP1受体而增强。最后，我们展示了这一点。尽管SIP促进了DNA的合成。高密度脂蛋白和高密度脂蛋白均不增加VSMC的细胞数。这些发现表明了一种通过其SIP组件(C)2004爱思唯尔爱尔兰有限公司的高密度脂蛋白抗动脉粥样硬化作用的新机制。保留所有权利。
High-density lipoprotein (HDL) is a well-established anti-risk factor against atherosclerosis. but the mechanism of its anti-atherogenic actions is not fully understood. Here, we examined the role of the HDL-associated sphingosine I-phosphate (SIP). a lysolipid mediator. in the lipoprotein-induced actions in rat vascular smooth muscle cells (VSMCs). Both HDL and SIP inhibited platelet-derived growth factor-induced migration of VSMCs. The inhibitory effect was associated with an inhibition of cell spreading and these responses were. reversed by a desensitization of VSMCs with SIP. HDL and SIP also inhibited migration of Chinese hamster ovary cells and this effect was enhanced by overexpressing SIP, receptor. Finally, we showed that. even though SIP promoted DNA synthesis. HDL and SIP did not increase cell number of VSMCs. These findings suggest a novel mechanism for anti-atherogenic actions of HDL through its SIP component (C) 2004 Elsevier Ireland Ltd. All rights reserved.