Journal
CIRCULATION
Volume 108, Issue 5, Pages 623-627Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/01.CIR.0000078642.45127.7B
Keywords
coagulation; inhibitors; endothelium-derived factors
Funding
- NHLBI NIH HHS [HL60782] Funding Source: Medline
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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 approximate to80%, 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 TFPIbeta/TFPIalpha mRNA of approximate to0.1 to 0.2. In Chinese hamster ovary (CHO) cells, TFPIalpha is predominantly secreted, whereas TFPIbeta is a GPI-anchored membrane protein. Like TFPIbeta, the small proportion of the TFPIalpha 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 (TFPIbeta) and indirect (TFPIalpha) GPI-mediated membrane anchorage is involved in localizing TFPI to the surface of cells.
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