Teuscher E, Pester E
Biomed Biochim Acta. 1984;43(4):447-56.
The observation that administration of antifibrinolytic drugs results in tumour growth stasis, having possibly its origin in reduced vascularization of the tumour, led us to investigate the migratory behaviour of bovine endothelial cells under in vitro conditions in the presence of drugs known to influence the activity of fibrinolytic enzymes. The Boyden-technique and microcinematography were used for this analysis. It could be shown that aprotinin, an inhibitor of serine proteinases and para-methylaminobenzoic acid, a specific inhibitor of plasminogen activation and plasmin action greatly reduced the migratory rate of the cells. Streptokinase, a plasminogen activator, stimulated the cell migration in optimal concentrations. The authors hypothesize that tumour vascularization is initiated by immigration of endothelial cells into the tumour by fibrinolytic action following a fibrin gradient induced by the tumour themselves. Fibrinolytic inhibitors suppress this process.
抗纤维蛋白溶解药物的给药导致肿瘤生长停滞，这一现象可能源于肿瘤血管生成减少，促使我们研究在体外条件下，已知会影响纤维蛋白溶解酶活性的药物存在时牛内皮细胞的迁移行为。为此分析采用了博伊登技术和显微电影摄影术。结果表明，丝氨酸蛋白酶抑制剂抑肽酶和纤溶酶原激活及纤溶作用的特异性抑制剂对甲基氨基苯甲酸能显著降低细胞的迁移率。纤溶酶原激活剂链激酶在最佳浓度下能刺激细胞迁移。作者推测，肿瘤血管生成是由内皮细胞在肿瘤自身诱导的纤维蛋白梯度作用下通过纤维蛋白溶解作用迁移到肿瘤中引发的。纤维蛋白溶解抑制剂会抑制这一过程。
