Glycosyl phosphatidylinositol anchorage of tissue factor pathway inhibitor.
Glycosyl phosphatidylinositol anchorage of tissue factor pathway inhibitor.
复制标题
组织因子途径抑制剂的糖基磷脂酰肌醇锚定。
DOI：
10.1161/01.cir.0000078642.45127.7b
复制
发表时间：
2003
期刊：
影响因子：
37.8
通讯作者：
BrozeJr,GeorgeJ
中科院分区：
文献类型：
--
作者：
Zhang,Jing;Piro,Orlando;Lu,Lan;BrozeJr,GeorgeJ
Background—The endothelium is a major source of tissue factor pathway inhibitor (TFPI), the endogenous regulator of TF-induced coagulation, and a significant proportion of the expressed TFPI remains associated with the endothelial surface.Methods and Results—Phosphatidylinositol-specific phospholipase C (PI-PLC) treatment reduced TFPI at the surface of cultured endothelial cells by ≈80%, and at least a portion of the TFPI released by PI-PLC contained an intrinsic glycosylphosphatidylinositol (GPI) anchor that is recognized by anti-crossreactive determinant antibodies. Endothelial cells express both of the alternatively spliced forms of TFPI mRNA at a ratio of TFPIβ/TFPIα mRNA of ≈0.1 to 0.2. In Chinese hamster ovary (CHO) cells, TFPIα is predominantly secreted, whereas TFPIβ is a GPI-anchored membrane protein. Like TFPIβ, the small proportion of the TFPIα expressed by CHO cells that remains surface associated is also released by PI-PLC treatment, suggesting that it is bound to a separate GPI-anchored protein(s) at the surface of the cells.Conclusions—Both direct (TFPIβ) and indirect (TFPIα) GPI-mediated membrane anchorage is involved in localizing TFPI to the surface of cells.
