EFFECTS OF ENDOTHELIAL-CELLS ON ACTIVITY OF STAPHYLOKINASE

Staphylokinase (SAK), produced by Staphylococcus aureus, induces fibri nolytic activity in circulation without systemic fibrinolytic activati on. Since the effect of blood vessels on the activity of SAK has not y et been clarified, plasminogen activator (PA) activity of SAK in the p resence or absence of endothelial cells was analyzed. The endothelial cells used in this experiment were of a cloned established cell line ( TKM-33). In the expression of PA activity by SAK or streptokinase (SK) , the kinetic constants revealed as Vmax/km were increased about 1.5-f old in the presence of endothelial cells. Furthermore, an initial lag phase which was observed during the plasminogen activation by SAK was markedly shortened in the presence of endothelial cells. In the case o f SK, an initial lag phase was not observed in the absence or presence of endothelial cells. Although PA activity of SAK was inhibited by al pha(2)-antiplasmin (alpha(2)-AP), the inhibitory effect of alpha(2)-AP in the presence of endothelial cells was weaker than in the absence o f endothelial cells. The cyanogen bromide digested fibrinogen fragment -2 (FCB-2) distinctly enhanced the PA activity of SAK in the absence a nd the presence of endothelial cells. However, alpha(2)-AP and FCB-2 d id not cause a significant alteration of PA activity of SK even in the absence or presence of endothelial cells. These findings suggest that PA activity of SAK is enhanced by endothelial cells, but inhibited by alpha(2)-AP. Moreover, PA activity of SAK is further enhanced by fibr in clot in the presence of endothelial cells.