| T112 |
0-1012 |
Sentence |
denotes |
The recruitment of leukocytes to a thrombus not only aids the immune response but also serves to facilitate platelet activation and coagulation.92 Activated platelets facilitate neutrophils to release NETs, which are a matrix of DNA decorated with neutrophils granule proteins, such as MPO (myeloperoxidase), cathepsin G, and neutrophil elastase.93,94 NETs appear to be a primary defence mechanism to invading pathogens and as such have been demonstrated to trap and kill bacteria and fungi in addition to sequestering viruses.94,95 However, NETs have also been implicated in the pathogenesis of arterial and venous thrombosis in addition to a range of pathologies, including disseminated intravascular coagulation, sepsis, preeclampsia, vasculitis, and systemic lupus erythematosus.96,97 In the context of thrombosis, the release of the highly negatively charged NETs can trap erythrocytes and activate platelets.98 Moreover, NETs serve as a scaffold and potent activator of coagulation via multiple mechanisms. |
| T113 |
1013-1610 |
Sentence |
denotes |
Indeed, neutrophil elastase associated with NETs degrades the anticoagulant protein, TFPI, thereby enhancing TF activity and thrombin generation.96 Histones activate platelets via TLR-2 and TLR-4 and enhance fibrin formation, while the contact activation system, via FXII activation, is initiated by negatively charged DNA.96,99 The activation of FXII not only initiates coagulation but also has important proinflammatory properties by way of its ability to liberate the generation of bradykinin, upregulate neutrophil function, and the generation of monocyte-derived proinflammatory cytokines.100 |
