Degradation of platelet-von Willebrand factor complexes by plasmin: an alternative/backup mechanism to ADAMTS13.
Degradation of platelet-von Willebrand factor complexes by plasmin: an alternative/backup mechanism to ADAMTS13.
复制标题
纤溶酶降解血小板-血管性血友病因子复合物：ADAMTS13 的替代/备用机制。
DOI：
10.1161/circulationaha.114.008298
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发表时间：
2014
期刊：
影响因子：
37.8
通讯作者：
Chauhan,AnilK
中科院分区：
文献类型：
--
作者：
Chauhan,AnilK
1274 Circulation March 25, 2014 multimers in a lysine-dependent manner in the absence of ADAMTS13 in vitro is exciting and is of great interest for research groups working in the ADAMTS13/VWF field. Previous studies12 have demonstrated the presence of platelet–VWF strings on the activated endothelium of Adamts13−/− mice. 12, 13 Therefore, it would be extremely interesting to determine whether infusion of plasminogen and streptokinase would prevent the formation of platelet–VWF strings in Adamts13−/− mice. This approach would help ascertain whether plasmin protects from murine TTP by acting as an alternative/backup VWF cleavage mechanism in vivo. It also would be interesting to determine whether infusion of plasminogen and streptokinase attenuates symptoms of acute TTP in Adamts13−/−(CASA/Rk background) mice challenged with bacterial toxin shigatoxin. 12 Such a finding might suggest a potential role for plasmin in protecting from hemolytic uremic syndrome, 14 as well as TTP.
