Nazih H, Devred D, Martin-Nizard F, Clavey V, Fruchart J C, Delbart C
Serlia: Institut Pasteur, Lille, France.
Thromb Res. 1992 Sep 1;67(5):559-67. doi: 10.1016/0049-3848(92)90016-4.
Initially we established that, in human platelets, low concentrations of HDL3 stimulate phosphatidylcholine (PC) hydrolysis and a transient increase in 1,2-diacylglycerol (DAG). In (3H) PC prelabelled platelets, phosphocholine is released into the medium during HDL3 induced PC turnover with a 1.5 to 2 fold increment, indicating that HDL3 stimulated DAG generation in platelets is likely due to phospholipase C (PLC). GTP or GTP-gamma-S augments, and pertussis toxin inhibits HDL3 stimulated DAG production. Treatment of platelet membranes with HDL3 or with proteoliposome containing apo A-I or A-II substantially prevents 41 kDa protein ADP-ribosylation that was induced by pertussis toxin, with apo A-II having an inhibitory potency greater than apo A-I. These data provide strong evidence that the pertussis sensible G protein (Go or Gi) is directly involved in coupling PLC to HDL3 receptor in platelets.
最初我们确定，在人血小板中，低浓度的HDL3刺激磷脂酰胆碱（PC）水解以及1,2 - 二酰甘油（DAG）短暂增加。在用（3H）PC预标记的血小板中，在HDL3诱导的PC周转过程中，磷酸胆碱以1.5至2倍的增量释放到培养基中，这表明HDL3刺激血小板中DAG的产生可能是由于磷脂酶C（PLC）。GTP或GTP-γ-S增强，而百日咳毒素抑制HDL3刺激的DAG产生。用HDL3或含有载脂蛋白A-I或A-II的蛋白脂质体处理血小板膜可显著阻止百日咳毒素诱导的41 kDa蛋白的ADP-核糖基化，其中载脂蛋白A-II的抑制效力大于载脂蛋白A-I。这些数据提供了强有力的证据，表明对百日咳敏感的G蛋白（Go或Gi）直接参与血小板中PLC与HDL3受体的偶联。
