ENHANCEMENT OF RESPIRATORY SYNCYTIAL VIRUS-INDUCED CYTOPATHOLOGY BY TRYPSIN, THROMBIN, AND PLASMIN
ENHANCEMENT OF RESPIRATORY SYNCYTIAL VIRUS-INDUCED CYTOPATHOLOGY BY TRYPSIN, THROMBIN, AND PLASMIN
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DOI：
10.1128/iai.40.1.351-358.1983
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发表时间：
1983-01-01
影响因子：
3.1
通讯作者：
TIDWELL, RR
中科院分区：
文献类型：
--
作者：
DUBOVI, EJ;GERATZ, JD;TIDWELL, RR
测试了一系列不同底物特异性的蛋白酶对呼吸道合胞病毒诱导的细胞病理学的影响。三种酶，凝血酶，纤溶酶和胰蛋白酶，显着增强病毒感染的A549 [人肺癌]细胞的融合。在浓度的基础上，凝血酶是最活跃的启动子，其次是纤溶酶，然后胰蛋白酶。水蛭素是一种特异性凝血酶抑制剂，它能阻断凝血酶的促融合作用，但对无凝血酶时的基础融合率无影响。相比之下，胰蛋白酶样蛋白酶的脒型抑制剂，双（5-脒基-2-苯并咪唑基）-甲烷（BABIM），不仅阻断了凝血酶的作用，而且阻断了无凝血酶对照组的融合。在低浓度下观察到BABIM的抑制活性，以排除对凝血酶本身的任何直接抑制作用。显然，凝血酶通过激活一种BABIM敏感的蛋白酶来促进细胞融合。可以预期纤溶酶和胰蛋白酶以类似的方式起作用。
A series of proteases of diverse substrate specificity were tested for their effect on respiratory syncytial virus-induced cytopathology. Three of the enzymes, thrombin, plasmin and trypsin, augmented significantly the fusion of virus-infected A549 [human lung carcinoma] cells. On a concentration basis, thrombin was the most active promoter, followed by plasmin and then trypsin. Hirudin, a specific thrombin inhibitor, blocked the fusion-enhanciong property of thrombin, yet had no influence on the basal rate of fusion in the absence of the enzyme. By contrast, the amidine-type inhibitors of trypsin-like proteases, bis(5-amidino-2-benzimidazolyl)-methane (BABIM), blocked not only the thrombin effect, but also the fusion in the thrombin-free controls. The suppressive activity of BABIM was observed at concentrations so low as to exclude any direct inhibitory effect on thrombin itself. Apparently, thrombin advances cell fusion by activating a BABIM-sensitive protease. Plasmin and trypsin can be expected to act in a similar manner.