细胞与凝血因子VII的激活

Cells and the activation of factor VII.

作者信息

Rao L V, Rapaport S I

机构信息

Department of Biochemistry, University of Texas Health Center at Tyler 75710, USA.

出版信息

Haemostasis. 1996;26 Suppl 1:1-5. doi: 10.1159/000217229.

DOI:10.1159/000217229

PMID:8904164

Abstract

Binding of factor VII to tissue factor (TF) present on or released from cells initiates TF-dependent coagulation in vivo. Earlier data obtained with relipidated TF suspensions led to the hypothesis that all factor VII bound to limiting TF sites exposed after tissue injury could be rapidly activated to VIIa/TF complexes by low concentrations of factor Xa, IXa, and VIIa. However, newer data on the activation of factor VII bound to TF expressed on cultured cell monolayers support the hypothesis that not all VII/TF complexes formed at a site of tissue injury are readily activated to VIIa/TF complexes during hemostasis. This is possibly related to why recombinant factor VIIa can bypass impaired IXa/VIIIa/phospholipid complex function in hemostasis.

摘要

凝血因子 VII 与细胞表面存在的或从细胞释放的组织因子 (TF) 结合，在体内启动 TF 依赖性凝血。早期使用重新脂质化的 TF 悬浮液获得的数据提出了这样的假设，即所有与组织损伤后暴露的有限 TF 位点结合的凝血因子 VII 可被低浓度的凝血因子 Xa、IXa 和 VIIa 迅速激活为 VIIa/TF 复合物。然而，关于结合在培养细胞单层上表达的 TF 的凝血因子 VII 激活的最新数据支持这样的假设，即在止血过程中，并非所有在组织损伤部位形成的 VII/TF 复合物都能轻易激活为 VIIa/TF 复合物。这可能与重组凝血因子 VIIa 能够在止血过程中绕过受损的 IXa/VIIIa/磷脂复合物功能的原因有关。