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Physiologic activities of the contact activation system
1Division of Hematology and Oncology, Case Western Reserve University, University Hospitals Case Medical Center, Cleveland, OH 44106, United States.
Thrombosis Research
|April 25, 2014
Summary
Genetic deletion of key proteins in the contact activation system (CAS) and kallikrein/kinin system (KKS) protects mice from thrombosis. This protection is linked to the renin-angiotensin system (RAS), not reduced contact activation.
Area of Science:
- Biochemistry
- Physiology
- Thrombosis Research
Background:
- The plasma contact activation system (CAS) and kallikrein/kinin system (KKS) involve factor XII, prekallikrein, high molecular weight kininogen, and the bradykinin B2 receptor.
- Genetic deficiencies in these components protect mice from thrombosis, suggesting a link to broader physiological pathways.
Purpose of the Study:
- To investigate the mechanisms underlying thrombosis protection in mice lacking components of the CAS and KKS.
- To explore the role of the renin-angiotensin system (RAS) in mediating thrombosis in these models.
Main Methods:
- Utilized murine genetic deletion models for factor XII (F12(-/-)), prekallikrein (Klkb1(-/-)), high molecular weight kininogen (Kgn1(-/-)), and the bradykinin B2 receptor (Bdkrb2(-/-)).
- Analyzed the contribution of the renin-angiotensin system (RAS) and prostacyclin pathways in thrombosis protection.
Main Results:
- Mice lacking Bdkrb2(-/-) showed protection from thrombosis via overexpression of RAS components, leading to increased prostacyclin and inhibited vascular/platelet activity.
- Prolylcarboxypeptidase deficiency resulted in a prothrombotic state, also partly mediated by the RAS.
Conclusions:
- Thrombosis in CAS and KKS deficient mice is significantly influenced by the renin-angiotensin system (RAS).
- The protective mechanisms observed are largely independent of reduced contact activation itself.
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