Aviram M, Brook J G
Atherosclerosis. 1983 Mar;46(3):259-68. doi: 10.1016/0021-9150(83)90176-4.
Gel-filtered platelets (GFP) from normal human subjects bound both low density lipoproteins (LDL) and high density lipoproteins (HDL). This binding was saturable and 125I-labelled lipoprotein uptake was inhibited by plasma. Platelets are also able to degrade lipoproteins but only to a limited extent. LDL appeared to compete with 125I-labelled HDL for platelet uptake, whereas the ability of HDL to displace 125I-LDL was limited. Cyclohexanedione-treated LDL (CHD-LDL), unlike CHD-HDL, did not compete with [125I]LDL for platelet accumulation, suggesting that arginine residues are necessary for LDL but not HDL binding. Addition of HDL or LDL to GFP did not alter platelet aggregation. However, in the presence of thrombin (0.5 U/ml), 1 mg/ml LDL incubated for 1 h at 23 degrees C enhanced platelet aggregation (215% increase) whereas HDL under similar conditions decreased aggregation by 53%. LDL also shortened the time of maximal aggregation whereas HDL had the opposite effect.
来自正常人类受试者的凝胶过滤血小板（GFP）能结合低密度脂蛋白（LDL）和高密度脂蛋白（HDL）。这种结合是可饱和的，血浆可抑制125I标记的脂蛋白摄取。血小板也能够降解脂蛋白，但程度有限。LDL似乎与125I标记的HDL竞争血小板摄取，而HDL置换125I-LDL的能力有限。环己二酮处理的LDL（CHD-LDL）与CHD-HDL不同，不与[125I]LDL竞争血小板蓄积，提示精氨酸残基对于LDL结合是必需的，但对于HDL结合并非必需。向GFP中添加HDL或LDL不会改变血小板聚集。然而，在凝血酶（0.5 U/ml）存在的情况下，1 mg/ml LDL于23℃孵育1小时可增强血小板聚集（增加215%），而在类似条件下HDL可使聚集降低53%。LDL还缩短了最大聚集时间，而HDL则有相反作用。
