Research Article

Cellular and Molecular Life Sciences CMLS

, Volume 62, Issue 13, pp 1514-1525

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

  • J. L. N. WolfsAffiliated withDepartment of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University
  • , P. ComfuriusAffiliated withDepartment of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University
  • , J. T. RasmussenAffiliated withProtein Chemistry Laboratory, Department of Molecular Biology, University of Aarhus
  • , J. F. W. KeurenAffiliated withSanquin, Blood Bank Region South-East
  • , T. LindhoutAffiliated withDepartment of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University
  • , R. F. A. ZwaalAffiliated withDepartment of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University
  • , E. M. BeversAffiliated withDepartment of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University Email author 

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Abstract.

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 Ca2+-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.

Key words.

Procoagulant activity scramblase aminophospholipid translocase thrombin collagen platelet phosphatidylserine microparticle