Makoveichuk E, Lookene A, Olivecrona G
Department of Medical Biochemistry and Biophysics, Umeâ University, Umeâ, Sweden.
Biochem Biophys Res Commun. 1998 Nov 27;252(3):703-10. doi: 10.1006/bbrc.1998.9596.
Lipoprotein lipase (LPL) is present in cells involved in development of atherosclerosis (endothelial cells, smooth muscle cells, and macrophages). A direct involvement of LPL in atherogenesis has been suggested. Previously we used the surface plasmon resonance technique to study the interaction of lipoproteins with surfaces covered by heparan sulfate proteoglycans (HSPG) and LPL [A. Lookene et al. (1997) Biochemistry 36, 5267-5275]. The binding was much increased by the presence of LPL. Here we demonstrate that mild oxidation of low-density-lipoprotein (LDL) and very-low-density lipoprotein (VLDL) in vitro increases their binding to surfaces covered by HSPG and LPL, while extensive oxidation decreases it. Similar results were obtained with a lipid emulsion (Intralipid), indicating that oxidation-induced changes of the lipid part could explain the effects. LPL increased binding and uptake of the mildly oxidized (compared to nonoxidized) LDL by THP-I monocyte-derived macrophages. Our studies indicate that LPL has the highest affinity for mildly oxidized LDL and support its involvement in development of atherosclerosis.
脂蛋白脂肪酶（LPL）存在于参与动脉粥样硬化发展的细胞中（内皮细胞、平滑肌细胞和巨噬细胞）。已有研究表明LPL直接参与动脉粥样硬化的形成。此前，我们使用表面等离子体共振技术研究脂蛋白与硫酸乙酰肝素蛋白聚糖（HSPG）和LPL覆盖的表面之间的相互作用[A. Lookene等人（1997年），《生物化学》36卷，5267 - 5275页]。LPL的存在显著增加了这种结合。在此我们证明，体外对低密度脂蛋白（LDL）和极低密度脂蛋白（VLDL）进行轻度氧化会增加它们与HSPG和LPL覆盖的表面的结合，而过度氧化则会降低这种结合。脂质乳剂（英脱利匹特）也得到了类似结果，表明脂质部分的氧化诱导变化可以解释这些效应。LPL增加了THP - 1单核细胞衍生巨噬细胞对轻度氧化（与未氧化相比）LDL的结合和摄取。我们的研究表明，LPL对轻度氧化的LDL具有最高亲和力，并支持其参与动脉粥样硬化的发展。
