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Role of vascular smooth muscle cells in the organization of a thrombus

血管平滑肌细胞在血栓组织中的作用

基本信息

批准号：
06670708
负责人：
NAITO Michitaka
金额：
$ 1.34万
依托单位：
Nagoya University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1994
资助国家：
日本
起止时间：
1994 至 1995
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-06670708/
关键词：
fibrinogen fibrin gel smooth muscle cell migration atherosclerosis thrombus organization factor XIII 血栓器質化フィブリン

项目摘要

We evaluated the migration of vascular smooth muscle cells into fibrin gels, using an in vitro assay system. Vascular smooth muscle cells from bovine fetal aorta migrated into fibrin gels and showed a characteristic elongated spindle-shaped appearance with long cytoplasmic processes.Varying the concentration of thrombin (0.05-1 NIHU/ml) used to form the fibrin gel had little effect on cell migration although higher concentrations of thrombin inhibited the migration. Migration of the cells into fibrin gels was dependent on RNA and protein synthesis but not on DNA synthesis. The addition of antithrombin III,hirudin, and D-phenylalanyl-L-prolyl-L-arginine chloromethyl ketone after gel formation had no effect, suggesting that residual thrombin in fibrin gels had no influence on subsequent cell migration. Neither the factor XIII-induced crosslinking of fibrin nor the fibrinopeptides released during gel formation were involved in the present migration assay system. Tranexamic acid, an inhibitor of plasminogen activator, or aprotinin, a plasmin inhibitor, also had no significant effect, suggesting that fibrinolysis induced by plasmin was not involved in this system. Theses findings showed that fibrin gels themselves induce the migration of vascular smooth muscle cells (haptotaxis) without other chemotactic or chemokinetic substances, suggesting an important role for fibrin in the development and progression of such vascular diseases as atherosclerosis, thrombosis and the development of restenosis following balloon angioplasty.

我们评估了血管平滑肌细胞迁移到纤维蛋白凝胶，使用体外分析系统。牛胎主动脉血管平滑肌细胞迁移到纤维蛋白凝胶中，表现出特征性的长梭形外观和长的胞质突起，形成纤维蛋白凝胶的凝血酶浓度（0.05-1 NIHU/ml）对细胞迁移几乎没有影响，但较高浓度的凝血酶抑制细胞迁移。细胞向纤维蛋白凝胶中的迁移依赖于RNA和蛋白质的合成，但不依赖于DNA的合成。在凝胶形成后加入抗凝血酶III、水蛭素和D-苯丙氨酰-L-脯氨酰-L-精氨酸氯甲基酮没有影响，表明纤维蛋白凝胶中残留的凝血酶对随后的细胞迁移没有影响。无论是因子XIII诱导的纤维蛋白交联，也没有在凝胶形成过程中释放的纤维蛋白肽参与本迁移试验系统。纤溶酶原激活物抑制剂氨甲环酸或纤溶酶抑制剂抑肽酶也没有显著影响，表明纤溶酶诱导的纤溶不参与该系统。这些发现表明，纤维蛋白凝胶本身诱导血管平滑肌细胞的迁移（趋触性），而不需要其他趋化或趋化动力学物质，这表明纤维蛋白在动脉粥样硬化、血栓形成和球囊血管成形术后再狭窄等血管疾病的发展和进展中起重要作用。