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高密度脂蛋白抑制牛主动脉内皮细胞对低密度脂蛋白的结合和摄取。

High density lipoprotein inhibits low density lipoprotein binding and uptake by bovine aortic endothelial cells.

作者信息

Alexander J J, Miguel R, Graham D

机构信息

Case Western Reserve University School of Medicine, Cleveland, Ohio.

出版信息

Angiology. 1990 Dec;41(12):1065-9. doi: 10.1177/000331979004101207.

DOI:10.1177/000331979004101207
PMID:2278402
Abstract

The antiatherogenic effect of high density lipoprotein (HDL) has been attributed to either an inhibition of cholesterol uptake or to reversed cholesterol transport from peripheral cells. In order to determine whether HDL competitively blocks receptor-mediated low density lipoprotein (LDL) binding and uptake, bovine aortic endothelial cells (BAECs) were cultured in Dulbecco's modified Eagles Medium (DMEM) containing 10% LDL-free fetal bovine serum, and incubated with 125I-LDL in concentrations of either 10 or 25 micrograms protein/mL. Varying amounts of HDL (0-200 micrograms/mL) were added to the media. Following a twenty-four hour incubation period at 37 degrees C, 125I-LDL binding and uptake were measured. At the lower concentration of 125I-LDL, which represents high-affinity receptor binding, there was no significant difference in either binding or uptake within the range of HDL concentrations studied. At the higher concentration of LDL, however, there was a marked inhibition of 125I-LDL binding (p less than .006) and uptake (p less than, 001; ANOVA), which did not saturate at the highest HDL concentrations used. These data suggest that HDL does not influence high-affinity, receptor-mediated binding and uptake of LDL but that its effect is seen at a concentration of LDL representing nonspecific binding. The lack of saturation at increasing concentrations of HDL also indicates that HDL-receptor interaction is not essential for the effect.

摘要

高密度脂蛋白(HDL)的抗动脉粥样硬化作用归因于对胆固醇摄取的抑制或外周细胞胆固醇逆向转运。为了确定HDL是否竞争性阻断受体介导的低密度脂蛋白(LDL)结合和摄取,将牛主动脉内皮细胞(BAECs)培养于含10%无LDL胎牛血清的杜尔贝科改良伊格尔培养基(DMEM)中,并用浓度为10或25微克蛋白/毫升的125I-LDL孵育。向培养基中加入不同量的HDL(0 - 200微克/毫升)。在37℃孵育24小时后,测量125I-LDL的结合和摄取。在较低浓度的125I-LDL(代表高亲和力受体结合)下,在所研究的HDL浓度范围内,结合或摄取均无显著差异。然而,在较高浓度的LDL下,125I-LDL的结合(p < 0.006)和摄取(p < 0.001;方差分析)受到显著抑制,且在所用的最高HDL浓度下未达到饱和。这些数据表明,HDL不影响高亲和力、受体介导的LDL结合和摄取,但其作用在代表非特异性结合的LDL浓度下可见。随着HDL浓度增加而缺乏饱和也表明HDL-受体相互作用对于该效应并非必需。

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HDL-Mediated Lipid Influx to Endothelial Cells Contributes to Regulating Intercellular Adhesion Molecule (ICAM)-1 Expression and eNOS Phosphorylation.高密度脂蛋白介导的脂质内流对内皮细胞调控细胞间黏附分子(ICAM-1)表达和内皮型一氧化氮合酶(eNOS)磷酸化的作用。
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