Lack of effect of serum amyloid A (SAA) on the ability of high-density lipoproteins to inhibit endothelial cell adhesion molecule expression
Lack of effect of serum amyloid A (SAA) on the ability of high-density lipoproteins to inhibit endothelial cell adhesion molecule expression
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DOI：
10.1016/s0021-9150(00)00437-8
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发表时间：
2001-01-01
期刊：
影响因子：
5.3
通讯作者：
Barter, PJ
中科院分区：
文献类型：
--
作者：
Ashby, D;Gamble, J;Barter, PJ
已经进行了研究，以确定高密度脂蛋白（HDL）抑制内皮细胞中细胞因子诱导的血管细胞粘附分子-1 （VCAM-1）表达的能力是否会因高密度脂蛋白中急性期反应物血清淀粉样蛋白- a （SAA）的存在而改变。19例患者分别在两次血浆中分离HDL3的制剂：第一次在冠状动脉搭桥术前收集，第二次在冠状动脉搭桥术后3天收集。术前HDL3样本中不含SAA，术后样本中SAA平均占HDL3蛋白的42%。术前HDL3和术后saa富集的HDL3在抑制人脐静脉内皮细胞（HUVECs）中肿瘤坏死因子- α (tnf - α)诱导的VCAM-1表达的能力方面是相同的。为了评估具有更大的SAA富集HDL3的效果，HDL3样品与纯化的SAA孵育，几乎取代了所有的apoAI和HDL3中约40%的apoAI。体外富集saa的HDL3以浓度依赖的方式抑制tnf - α诱导的HUVECs中VCAM-1的表达，与未修饰的HDL3相同。SAA的存在并未改变HDL3与内皮细胞的细胞表面结合。由此得出结论，HDL中SAA的存在对这些脂蛋白抑制内皮细胞中VCAM-1表达或与内皮细胞表面蛋白结合的能力没有影响。(C) 2001爱思唯尔科学爱尔兰有限公司版权所有。
Studies have been conducted to determine whether the ability of high density lipoproteins (HDL) to inhibit the cytokine-induced expression of vascular cell adhesion molecule-1 (VCAM-1) in endothelial cells is altered by the presence in HDL of the acute phase reactant, serum amyloid-A (SAA). Preparations of HDL3 were isolated on two separate occasions from the plasma of each of 19 patients: the first was collected before and the second 3 days after undergoing coronary artery bypass graft surgery. Whereas the preoperative HDL3 sample contained no SAA, in the postoperative sample SAA accounted for an average of 42% of the HDL3 protein. The preoperative HDL3 and postoperative, SAA-enriched HDL3 were identical in terms of their ability to inhibit the tumour necrosis factor-alpha (TNF-alpha)-induced expression of VCAM-1 in human umbilical vein endothelial cells (HUVECs). To assess the effect of having an even greater SAA enrichment of HDL3, samples of HDL3 were incubated with purified SAA, which displaced almost all of the apoAI and about 40% of the apoAII from the HDL3. This in vitro SAA-enriched HDL3 inhibited the TNF-alpha -induced expression of VCAM-1 in HUVECs in a concentration dependent manner, which was identical to that of the unmodified HDL3. The presence of SAA did not alter the cell-surface binding of HDL3 to endothelial cells. It has been concluded that the presence of SAA in HDL has no effect on the ability of these lipoproteins either to inhibit the expression of VCAM-1 in endothelial cells or to bind to proteins on the endothelial cell surface. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.