Ikeda K, Nagasawa K, Horiuchi T, Tsuru T, Nishizaka H, Niho Y
First Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Thromb Haemost. 1997 Feb;77(2):394-8.
Tissue factor (TF) is an integral membrane glycoprotein that serves as a cofactor for blood coagulation factor VIIa. The induction of TF on the surface of endothelial cells is initiated by various stimuli including lipopolysaccharide, interleukin-1 beta, and tumor necrosis factor alpha. We have demonstrated that recombinant human C5a induces TF activity in a dose-dependent fashion in human umbilical vein endothelial cells (HUVEC). Peak activity (4.9-fold increase) was obtained 3-6 h after treatment with 10 microM C5a. TF mRNA as assessed by RT-PCR method was also significantly increased (3.75-fold) after 3 h incubation with C5a, suggesting that C5a induces TF activity on HUVEC, at least in part, by enhancing the level of TF mRNA. The increase in TF activity by C5a was inhibited by methylprednisolone. The induction of TF on endothelial cells by C5a may represent one of many potential interrelationships between the inflammatory and coagulation schemes.
组织因子(TF)是一种整合膜糖蛋白,作为凝血因子VIIa的辅因子。内皮细胞表面TF的诱导由多种刺激引发,包括脂多糖、白细胞介素-1β和肿瘤坏死因子α。我们已经证明,重组人C5a以剂量依赖的方式在人脐静脉内皮细胞(HUVEC)中诱导TF活性。用10 microM C5a处理3-6小时后获得峰值活性(增加4.9倍)。用RT-PCR方法评估,与C5a孵育3小时后TF mRNA也显著增加(3.75倍),表明C5a至少部分地通过提高TF mRNA水平在HUVEC上诱导TF活性。C5a引起的TF活性增加被甲基泼尼松龙抑制。C5a在内皮细胞上诱导TF可能代表炎症和凝血机制之间许多潜在相互关系之一。