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首页> 外文期刊>Pathobiology: journal of immunopathology, molecular and cellular biology >Anionic peptide factor/phosphatidylcholine particles promote the inhibition of vascular cell adhesion molecule-1 in human umbilical vein endothelial cells.
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Anionic peptide factor/phosphatidylcholine particles promote the inhibition of vascular cell adhesion molecule-1 in human umbilical vein endothelial cells.

机译：阴离子肽因子/磷脂酰胆碱颗粒可促进人脐静脉内皮细胞中血管细胞粘附分子-1的抑制。

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OBJECTIVE: High-density lipoproteins (HDLs) have significant cardiovascular benefits by retarding the progression of atherosclerosis. One of the mechanisms is the inhibition by HDLs of the vascular cell adhesion molecule-1 (VCAM-1) expression in endothelial cells. Our objective was to test the effect on VCAM-1 expression by the human umbilical vein endothelial cells (HUVEC) of a minor HDL2 and HDL3 apolipoprotein, the anionic peptide factor (APF). The peptide has previously been found to develop some beneficial effects against atherosclerosis, i.e. by promoting the cholesterol efflux from endothelial cells. METHODS: We examined the effects of two HDL apolipoproteins A-I and APF, either in presence or absence of phosphatidylcholines (PCs), or free PCs, on the expression of VCAM-1 by HUVEC. The cells were stimulated with either the tumor necrosis factor-alpha (TNFalpha, 500 pg/ml) or the calcium bound to heparin (10 microg Ca2+/ml, 50 microg heparin/ml). RESULTS: In the presence of TNFalpha, only the free PCs (0.25 and 1 mM) developed an inhibitory effect (up to 50%). In the absence of TNFalpha and in the presence of calcium bound to heparin, either the lipid-free APF (3.5 microM) or the APF/PC complexes (1:57 molar ratio) or the free PCs (0.25 mM) exhibited a substantial inhibitory effect (72, 71 and 42%, respectively). CONCLUSION: Our present findings suggest for the first time that one of the mechanisms of the antiatherogenic action of APF involves the inhibition of VCAM-1 expression by HUVEC. The peptide, through its phospholipid-binding and its calcium antagonist abilities, appears to confer on the HDLs a protective effect against the early cellular event of the inflammatory process.
机译：目的：高密度脂蛋白（HDLs）通过延缓动脉粥样硬化的发展而具有明显的心血管益处。机制之一是通过HDL抑制内皮细胞中血管细胞粘附分子1（VCAM-1）的表达。我们的目标是测试次要HDL2和HDL3载脂蛋白（阴离子肽因子（APF））对人脐静脉内皮细胞（HUVEC）对VCAM-1表达的影响。先前已经发现该肽对动脉粥样硬化具有某些有益作用，即通过促进内皮细胞的胆固醇流出。方法：我们检查了两种HDL载脂蛋白A-1和APF在有无磷脂酰胆碱（PCs）或游离PC存在下对HUVEC对VCAM-1表达的影响。用肿瘤坏死因子-α（TNFalpha，500 pg / ml）或结合肝素的钙（10 microg Ca2 + / ml，50 microg肝素/ ml）刺激细胞。结果：在存在TNFalpha的情况下，只有游离PC（0.25和1 mM）产生抑制作用（高达50％）。在没有TNFα且钙与肝素结合的情况下，无脂质的APF（3.5 microM）或APF / PC复合物（1:57摩尔比）或游离的PC（0.25 mM）都表现出明显的抑制作用效果（分别为72％，71％和42％）。结论：我们目前的发现首次表明，APF的抗动脉粥样硬化作用机制之一涉及HUVEC抑制VCAM-1表达。该肽通过其磷脂结合和其钙拮抗剂的功能，似乎赋予了HDL抵抗炎症过程早期细胞事件的保护作用。

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