Changes in markers of vascular injury in response to transient hyperhomocysteinemia.
Changes in markers of vascular injury in response to transient hyperhomocysteinemia.
复制标题
短暂性高同型半胱氨酸血症引起的血管损伤标志物的变化。
DOI：
10.1053/meta.2003.50081
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发表时间：
2003
期刊：
影响因子：
--
通讯作者：
Roberts,JamesM
中科院分区：
文献类型：
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作者：
Powers,RobertW;Majors,AlanaK;Cerula,StacyL;Huber,HeatherA;Schmidt,BrianP;Roberts,JamesM
本研究的目的是测试同型半胱氨酸的瞬时增加是否会促进内皮损伤标志物细胞纤连蛋白（cFN）和可溶性血管细胞粘附分子1（sVCAM-1）的变化。在人类受试者中，同型半胱氨酸、cFN和sVCAM-1浓度响应于6小时的甲硫氨酸负荷而显著增加。然而，同型半胱氨酸和cFN或sVCAM-1之间没有观察到相关性。为了直接测试同型半胱氨酸是否可以损伤内皮细胞，将人脐静脉内皮细胞（HUVEC）与来自高同型半胱氨酸血症小鼠或来自甲硫氨酸负载的测试受试者的浓度增加的同型半胱氨酸、血浆或血清一起孵育。高同型半胱氨酸血症转基因小鼠的血浆（而非血清）培养的内皮细胞或蛋氨酸负载的人类受试者的cFN释放增加。这些数据表明，非常高的同型半胱氨酸浓度可以促进内皮损伤;然而，这种效应可能是由继发性效应介导的，包括血浆中存在的影响内皮细胞的因子。
The purpose of this study was to test whether transient increases in homocysteine would promote changes in markers of endothelial injury, cellular fibronectin (cFN), and soluble vascular cell adhesion molecule 1 (sVCAM-1). Homocysteine, cFN, and sVCAM-1 concentrations increased significantly in response to a methionine load by 6 hours in human subjects. However, no correlation was observed between homocysteine and cFN or sVCAM-1. To directly test whether homocysteine can injure endothelial cells, human umbilical vein endothelial cells (HUVEC) were incubated with increasing concentrations of homocysteine, plasma, or serum from hyperhomocysteinemic mice or from the methionine-loaded test subjects. cFN release was increased from endothelial cells cultured with plasma (but not serum) of hyperhomocysteinemic transgenic mice or from methionine-loaded human subjects. These data suggest that very high homocysteine concentrations can promote endothelial injury; however, this effect is likely mediated by secondary effects that include a factor(s) present in plasma that affects endothelial cells.