Pro‐urokinase and prekallikrein are both associated with platelets

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Abstract
The contact‐dependent intrinsic pathway of fibrinolysis involving factor XII, prekallikrein (PK) and pro‐urokinase (pro‐UK) remains poorly understood. Casein autography of washed, intact platelets revealed both PK and pro‐UK. Accordingly, platelets may mediate physiological thrombolysis by this pathway since factor XIIa activates PK and kallikrein activates pro‐UK. Acid washing dissociated PK but not pro‐UK from platelets. Exogenous pro‐UK was specifically incorporated by platelets from the ambient fluid and similarly could not be dissociated from intact platelets. Therefore, platelets may also mediate an effect from therapeutically administered pro‐UK by prolonging its half‐life.