Greilberger J, Jürgens G
Institute of Medical Biochemistry, Karl-Franzens Universität Graz, Harrachgasse 21, A-8010 Graz, Austria.
Biochem J. 1998 Apr 1;331 ( Pt 1)(Pt 1):185-91. doi: 10.1042/bj3310185.
The changes in the immunological properties of apolipoprotein AI (apo-AI) and AII (apo-AII) during the oxidation of the high-density lipoprotein HDL3 and its influence on the binding of heavily oxidized low-density lipoprotein (LDL) to type I and III collagen were investigated. Oxidation of HDL3 or Eu3+-labelled HDL3 was performed with CuSO4, varying the time of oxidation. Oxidation of HDL3 resulted in an increase in lipid hydroperoxides and enhanced the negative charge of this lipoprotein. Immunological studies with a solid-phase sandwich immunoassay revealed a strong increase in binding of Eu3+-labelled HDL3 to polyclonal antibodies against apo-AI and apo-AII within the first 4 h of oxidation. Neo-epitopes were also formed by interaction of the apolipoproteins with degradation products from the lipid peroxidation of polyunsaturated fatty acids, as evidenced by an immunoreaction of oxidized Eu3+-labelled HDL3 with antibodies to 4-hydroxynonenal (4-HNE)- and malondialdehyde (MDA)-protein adducts. Western blot analysis of oxidized HDL3 samples showed, as well as apo-AI and apo-AII bands, larger aggregated apolipoproteins, occurring after 0.5-2.5 h of oxidation. These aggregates were recognized by antibodies to apo-AI and apo-AII as well as by antibodies to 4-HNE- and MDA-protein adducts. Furthermore the original apo-AI monomers and apo-AII dimers decreased during the oxidation. The ability of native and oxidized HDL3 to prevent the binding of Eu3+-labelled 24 h-oxidized LDL to collagen on microtitration plates was estimated. Interestingly, 2 h-oxidized HDL3 competed most with the binding of 24 h-oxidized LDL on collagen type I and type III, followed by native HDL3. However, 24 h-oxidized HDL3 was a weaker competitor. Thus oxidative modification of HDL3 strongly alters the immunological properties of this lipoprotein and its binding affinity for collagen.
研究了高密度脂蛋白HDL3氧化过程中载脂蛋白AI(apo-AI)和AII(apo-AII)免疫特性的变化及其对高度氧化的低密度脂蛋白(LDL)与I型和III型胶原结合的影响。用CuSO4对HDL3或Eu3+标记的HDL3进行氧化,改变氧化时间。HDL3的氧化导致脂质氢过氧化物增加,并增强了该脂蛋白的负电荷。采用固相夹心免疫分析法进行的免疫学研究表明,在氧化的最初4小时内,Eu3+标记的HDL3与抗apo-AI和apo-AII多克隆抗体的结合显著增加。载脂蛋白与多不饱和脂肪酸脂质过氧化降解产物相互作用也形成了新表位,氧化的Eu3+标记HDL3与抗4-羟基壬烯醛(4-HNE)和丙二醛(MDA)-蛋白质加合物抗体的免疫反应证明了这一点。氧化HDL3样品的蛋白质印迹分析显示,除了apo-AI和apo-AII条带外,氧化0.5 - 2.5小时后出现了更大的聚集载脂蛋白。这些聚集体可被抗apo-AI和apo-AII抗体以及抗4-HNE和MDA-蛋白质加合物抗体识别。此外,在氧化过程中原有的apo-AI单体和apo-AII二聚体减少。评估了天然和氧化HDL3在微量滴定板上阻止Eu3+标记的24小时氧化LDL与胶原结合的能力。有趣的是,2小时氧化的HDL3在I型和III型胶原上与24小时氧化LDL的结合竞争最强,其次是天然HDL3。然而,24小时氧化的HDL3是较弱的竞争者。因此,HDL3的氧化修饰强烈改变了该脂蛋白的免疫特性及其与胶原的结合亲和力。