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Platelet-coagulant protein interactions in contact activation
Annals of the New York Academy of Sciences
|January 1, 1981
Summary
Human platelets activate factor XII and factor XI through distinct mechanisms. Platelets promote factor XII activation and factor XI activation via both factor XII-dependent and independent pathways.
Area of Science:
- Hematology
- Biochemistry
- Molecular Biology
Background:
- Platelets are known to influence blood coagulation.
- Previous research suggested two platelet-mediated pathways for factor XI activation, involving factor XII or collagen.
- The precise mechanisms remained unclear.
Purpose of the Study:
- To investigate the mechanisms by which human platelets promote the activation of factor XII and factor XI.
- To elucidate the roles of factor XII, high molecular weight kininogen, and kallikrein in platelet-mediated coagulation activation.
Main Methods:
- Utilized purified factors XII and XI, alongside kallikrein and high molecular weight kininogen.
- Employed ADP- or collagen-treated platelets in various combinations.
- Assessed proteolytic cleavage of factors XII and XI, and factor XIIa coagulant activity.
Main Results:
- ADP- or collagen-treated platelets facilitated factor XII activation by kallikrein and high molecular weight kininogen.
- Platelets participated with high molecular weight kininogen and kallikrein in factor XI activation.
- Factor XI activation was shown to be partially dependent on and partially independent of factor XII.
Conclusions:
- Human platelets can promote the proteolytic activation of factor XII via kallikrein.
- Platelets mediate factor XI activation through both factor XII-dependent and factor XII-independent pathways.
- These findings clarify platelet involvement in the intrinsic coagulation cascade.