Fyrnys B, Blencowe C, Deigner H P
Pharmazeutisch-Chemisches Institut, Universität Heidelberg, Germany.
FEBS Lett. 1995 Jan 2;357(1):7-12. doi: 10.1016/0014-5793(94)01312-o.
Addition of the phospholipids 1-O-hexadecyl-2-arachidonoyl-sn-glycero-3-phosphocholine (PLE) and 1-O-hexa-decyl-2-desoxy-2-amino-arachidonyl-sn-glycero-3- phosphocholine (PLA) to [125I]LDL and subsequent Cu(2+)-induced oxidation result in significant differences in protein modification and uptake by P388D1 macrophage-like cells. PLE-treated LDL is ingested at a 1.27-fold rate compared to PLE-treated LDL and displays enhanced electrophilic mobility. Similar results (1.43-fold enhanced uptake of LDL preloaded with PLE) are obtained when the uptake of phospholipid-enriched oxLDL particles are examined. The preference for ingestion as well as protein modification of both preparations is, however, reversed under experimental conditions allowing diffusion and inactivation of a fraction of the peroxidation products. These findings suggest that LDL-associated PAF-acetylhydrolase can exert a dual role and, to be protective to LDL, require an appropriate microenvironment, capable of binding certain species of oxidatively fragmented lipids.
向[125I]低密度脂蛋白（LDL）中添加磷脂1-O-十六烷基-2-花生四烯酰基-sn-甘油-3-磷酸胆碱（PLE）和1-O-十六烷基-2-脱氧-2-氨基花生四烯酰基-sn-甘油-3-磷酸胆碱（PLA），随后经铜（2+）诱导氧化，会导致P388D1巨噬细胞样细胞在蛋白质修饰和摄取方面出现显著差异。与未处理的LDL相比，经PLE处理的LDL的摄取速率提高了1.27倍，且显示出增强的电泳迁移率。当检测富含磷脂的氧化型LDL颗粒的摄取情况时，也得到了类似的结果（预加载PLE的LDL摄取增强了1.43倍）。然而，在允许一部分过氧化产物扩散和失活的实验条件下，两种制剂在摄取偏好以及蛋白质修饰方面的情况则相反。这些发现表明，与LDL相关的血小板活化因子乙酰水解酶可以发挥双重作用，并且要对LDL起到保护作用，需要一个能够结合某些氧化片段化脂质种类的合适微环境。
