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暴露于氧化型低密度脂蛋白的人内皮细胞黏附分子的表达。氧化程度和氧化型低密度脂蛋白位置的影响。

Expression of adhesion molecules by human endothelial cells exposed to oxidized low density lipoprotein. Influences of degree of oxidation and location of oxidized LDL.

作者信息

Takei A, Huang Y, Lopes-Virella M F

机构信息

Department of Medicine, Kgusha University, Fukuoka, Japan.

出版信息

Atherosclerosis. 2001 Jan;154(1):79-86. doi: 10.1016/s0021-9150(00)00465-2.

Abstract

The main objective of this study was to determine the influence of the degree of low density lipoprotein (LDL) oxidation and the location of oxidized LDL (oxLDL) on expression of adhesion molecules on endothelial cells (EC). OxLDL preparations 1-4 with different degrees of oxidative modification were studied. All preparations of oxLDL, after addition to the medium, stimulated the expression of intercellular adhesion molecule-1 (ICAM-1) by human umbilical vein endothelial cells (HUVEC) as determined by cell-ELISA. Concentration-dependent studies examining ICAM-1 expression by HUVEC showed that the minimal concentration of oxLDL which significantly stimulated ICAM-1 expression was 5 microg/ml, suggesting that the predicted physiological concentration of oxLDL in plasma may be not high enough to elicit a substantial increase of ICAM-1 expression in EC. In contrast, very small amounts (0.15 microg/well) of oxLDL-3 and 4, the more heavily oxidized LDL preparations, stimulated effectively ICAM-1 expression by HUVEC when located below the endothelial cell monolayer by immobilizing to type I collagen. The results suggest that the increased expression of ICAM-1 induced by accumulated oxLDL may be one of the mechanisms by which oxLDL contributes to atherogenesis.

摘要

本研究的主要目的是确定低密度脂蛋白(LDL)氧化程度及氧化型LDL(oxLDL)的位置对内皮细胞(EC)上黏附分子表达的影响。研究了具有不同氧化修饰程度的oxLDL制剂1 - 4。通过细胞酶联免疫吸附测定法(cell - ELISA)确定,所有oxLDL制剂加入培养基后,均可刺激人脐静脉内皮细胞(HUVEC)表达细胞间黏附分子 - 1(ICAM - 1)。对HUVEC中ICAM - 1表达进行的浓度依赖性研究表明,能显著刺激ICAM - 1表达的oxLDL最低浓度为5微克/毫升,这表明血浆中oxLDL的预测生理浓度可能不足以引起EC中ICAM - 1表达的显著增加。相反,极少量(0.15微克/孔)的oxLDL - 3和4(氧化程度更高的LDL制剂),通过固定在I型胶原上位于内皮细胞单层下方时,可有效刺激HUVEC表达ICAM - 1。结果表明,累积的oxLDL诱导ICAM - 1表达增加可能是oxLDL促进动脉粥样硬化形成的机制之一。

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