TMEM16F-Mediated Platelet Membrane Phospholipid Scrambling Is Critical for Hemostasis and Thrombosis but not Thromboinflammation in Mice: Brief Report

Ayesha A. Baig, Elizabeth J. Haining, Eva Geuss, Sarah Beck, Frauke Swieringa, Podchanart Wanitchakool, Michael K. Schuhmann, David Stegner, Karl Kunzelmann, Christoph Kleinschnitz, Johan W. M. Heemskerk, Attila Braun, Bernhard Nieswandt*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

34 Citations (Web of Science)


Objective-It is known that both platelets and coagulation strongly influence infarct progression after ischemic stroke, but the mechanisms and their interplay are unknown. Our aim was to assess the contribution of the procoagulant platelet surface, and thus platelet-driven thrombin generation, to the progression of thromboinflammation in the ischemic brain. Approach and Results-We present the characterization of a novel platelet and megakaryocyte-specific TMEM16F (anoctamin 6) knockout mouse. Reflecting Scott syndrome, platelets from the knockout mouse had a significant reduction in procoagulant characteristics that altered thrombin and fibrin generation kinetics. In addition, knockout mice showed significant defects in hemostasis and arterial thrombus formation. However, infarct volumes in a model of ischemic stroke were comparable with wild-type mice. Conclusions-Platelet TMEM16F activity contributes significantly to hemostasis and thrombosis but not cerebral thromboinflammation. These results highlight another key difference between the roles of platelets and coagulation in these processes.
Original languageEnglish
Pages (from-to)2152-2157
JournalArteriosclerosis Thrombosis and Vascular Biology
Issue number11
Publication statusPublished - Nov 2016


  • blood platelets
  • fibrin
  • stroke
  • thrombin
  • thrombosis

Cite this