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Staphylokinase reduces plasmin formation by endogenous plasminogen activators
Tao Jin1, Maria Bokarewa, Yihong Zhu
1Department of Rheumatology and Inflammation Research, Sahlgrenska University Hospital, Göteborg, Sweden. tao.jin@rheuma.gu.se
European Journal of Haematology
|March 12, 2008
Summary
Staphylokinase (SAK) inhibits plasminogen (Plg) activation by tissue-type or urokinase-type plasminogen activators (tPA/uPA). This bacterial protein reduces fibrinolysis by forming a SAK.Plg complex, counteracting bleeding risks.
Area of Science:
- Biochemistry
- Hematology
- Molecular Biology
Background:
- Hyperfibrinolysis results from an imbalance between fibrinolytic activators and inhibitors.
- Elevated levels of plasminogen (Plg) activators like tissue-type (tPA) or urokinase-type (uPA) plasminogen activators are primary causes of hyperfibrinolysis and can lead to hemorrhages.
Purpose of the Study:
- To investigate the effect of staphylokinase (SAK) on plasminogen (Plg) activation mediated by endogenous tPA and uPA.
- To elucidate the mechanism by which SAK influences tPA/uPA-induced fibrinolysis.
Main Methods:
- Assessing the impact of SAK on Plg activation in the presence of tPA and uPA.
- Investigating the interaction between SAK, Plg, tPA, uPA, and human neutrophil peptides (HNPs).
- Analyzing the role of SAK's NH2-terminal residues in its inhibitory function.
Main Results:
- Staphylokinase (SAK) was found to inhibit Plg activation mediated by tPA and uPA.
- SAK directly acts on Plg, forming a SAK.Plg complex, which reduces Plg-dependent fibrinolysis.
- The inhibitory effect of SAK is abrogated by interaction with HNPs, and its NH2-terminal residues are crucial for this inhibition.
Conclusions:
- SAK downregulates tPA/uPA-induced fibrinolysis through the formation of a SAK.Plg complex.
- This mechanism offers a potential strategy for managing hyperfibrinolysis and associated bleeding complications.
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