凝血酶诱导PAR1介导的快速非经典成纤维细胞生长因子1释放。
Thrombin induces rapid PAR1-mediated non-classical FGF1 release.
作者信息
Duarte Maria, Kolev Vihren, Soldi Raffaella, Kirov Alexander, Graziani Irene, Oliveira Silvia Marta, Kacer Doreen, Friesel Robert, Maciag Thomas, Prudovsky Igor
机构信息
Maine Medical Center Research Institute, 81 Research Drive, Scarborough, ME 04074, USA.
出版信息
Biochem Biophys Res Commun. 2006 Nov 24;350(3):604-9. doi: 10.1016/j.bbrc.2006.09.107. Epub 2006 Sep 28.
Abstract
Thrombin induces cell proliferation and migration during vascular injury. We report that thrombin rapidly stimulated expression and release of the pro-angiogenic polypeptide fibroblast growth factor 1 (FGF1). Thrombin failed to induce FGF1 release from protease-activated receptor 1 (PAR1) null fibroblasts, indicating that this effect was dependent on PAR1. Similarly to thrombin, FGF1 expression and release were induced by TRAP, a specific oligopeptide agonist of PAR1. These results identify a novel aspect of the crosstalk between FGF and thrombin signaling pathways which both play important roles in tissue repair and angiogenesis.
摘要
凝血酶在血管损伤时诱导细胞增殖和迁移。我们报告凝血酶迅速刺激促血管生成多肽成纤维细胞生长因子1（FGF1）的表达和释放。凝血酶不能从蛋白酶激活受体1（PAR1）缺失的成纤维细胞中诱导FGF1释放，表明这种作用依赖于PAR1。与凝血酶类似，FGF1的表达和释放由PAR1的特异性寡肽激动剂TRAP诱导。这些结果揭示了FGF和凝血酶信号通路之间相互作用的一个新方面，这两条信号通路在组织修复和血管生成中都发挥着重要作用。
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