|Molecular mass||92 000 Da|
|Half-life||2.2 days Glu-plasminogen |
0.8 days Lys-plasminogen
|Plasma concentration||0.2 g/l, 3.5 CTA U/ml|
|Normal range||70 - 140%|
|Primary structure||791 amino acids|
Plasminogen is the inactive precursor (proenzyme) of plasmin, the central protease in the fibrinolytic system. The binding of plasminogen to fibrin via lysin binding sites is followed by its activation to plasmin by urokinase (u-PA), tissue-type plasminogen activator (t-PA) or kallikrein. Single-chain plasminogen is thereby cleaved into two-chain plasmin. Plasmin is able to cleave Glu-plasminogen (N-terminal glutamic acid) into Lys-plasminogen (N-terminal lysin). It is suspected that this accelerates the activation of plasminogen by t-PA. Plasmin is inhibited by the plasmin inhibitor (α2-antiplasmin) and histidine-rich glycoprotein (HRG), which forms a reversible complex with plasmin/plasminogen.
Hereditary plasminogen deficiency (dysplasminogenemia) represents an increased risk for venous thromboembolism and reocclusion. An acquired plasminogen deficiency has been observed as a consecutive symptom in fibrinolytic therapy (e.g. with streptokinase), DIC, hepatic disease, sepsis, leukaemia and following surgery. In septic patients, the reduction of plasminogen is due to its cleavage by leukocyte elastase. Increased plasminogen levels are observed in acute phases (e.g. inflammation) during pregnancy, during the intake of oral contraceptives and following liver and kidney transplantations before rejection reactions.
- At the onset of a fibrinolytic therapy
- In consumption coagulopathies (DIC)
- Determination of the fibrinolytic potential
- Venous thromboembolism of unknown reason
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