Activated scramblase and inhibited aminophospholipid translocase cause phosphatidylserine exposure in a distinct platelet fraction

被引:87
作者
Wolfs, JLN
Comfurius, P
Rasmussen, JT
Keuren, JFW
Lindhout, T
Zwaal, RFA
Bevers, EM
机构
[1] Maastricht Univ, Cardiovasc Res Inst Maastricht, Dept Biochem, NL-6200 MD Maastricht, Netherlands
[2] Univ Aarhus, Dept Mol Biol, Prot Chem Lab, DK-8000 Aarhus, Denmark
[3] Sanquin, Blood Bank Reg SE, Maastricht, Netherlands
关键词
procoagulant activity; scramblase; aminophospholipid translocase; thrombin; collagen; platelet; phosphatidylserine; microparticle;
D O I
10.1007/s00018-005-5099-y
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Platelet procoagulant activity is mainly determined by the extent of surface-exposed phosphatidylserine (PS), controlled by the activity of aminophospholipid translocase and phospholipid scramblase. Here, we studied both transport activities in single platelets upon stimulation with various agonists. Besides the formation of procoagulant microparticles, the results show that a distinct fraction of the platelets exposes PS when stimulated. The extent of PS exposure in these platelet fractions was similar to that in platelets challenged with Ca(2+)-ionophore, where all cells exhibit maximal attainable PS exposure. The size of the PS-exposing fraction depends on the agonist and is proportional to the platelet procoagulant activity Scramblase activity was observed only in the PS-exposing platelet fraction, whereas translocase activity was exclusively detectable in the fraction that did not expose PS. We conclude that, irrespective of the agonist, procoagulant platelets exhibit maximal surface exposure of PS by switching on scramblase and inhibiting translocase activity.
引用
收藏
页码:1514 / 1525
页数:12
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