Grant-in-Aid for Scientific Research (C)
We observed that sphingomyelin (SM)-rich rafts are identified histochemically in the central region of adhered platelets where fibrin is colocalized on activation by thrombin. The clot retraction of SM-depleted platelets from SM synthase knockout mouse was delayed significantly, suggesting that platelet SM-rich rafts are involved in clot retraction. Furthermore, fibrin translocation to DRM rafts was impaired in factor XIII A subunit-deficient mouse platelets, which show impaired clot retraction. Furthermore, the disruption of SM-rich rafts by methyl-β-cyclodextrin impaired clot retraction. Thus, we propose that clot retraction takes place in SM-rich rafts where a fibrin-αIIbβ3 complex is formed as a primary axis to promote platelet contraction.
Japanese Journal of Thrombosis and Hemostasis
Jpn. J. Clin. Hematol.
Eur. Phys. J. E
Attribution of KAKENHI