Binding of urinary protein C inhibitor to fibrin(ogen) and its binding mechanism

Blood Coagul Fibrinolysis. 1993 Feb;4(1):153-8.

Abstract

The region and mechanism of urinary protein C inhibitor (PCI) binding to fibrin(ogen) were examined using fibrin(ogen)-Sepharose and ligand blotting. Urinary PCI bound to fibrin(ogen)-Sepharose in a heparin-dependent manner at a level about 1.6-fold higher to fibrin-Sepharose than to fibrinogen-Sepharose. Scatchard analysis of the binding between urinary PCI and fibrin(ogen)-Sepharose showed that the Kd for fibrin-Sepharose and fibrinogen-Sepharose were 4.0 nM and 5.7 nM respectively. Ligand blotting using urinary PCI and an enzyme-linked immunoassay showed that urinary PCI bound to fibrinogen, fibrinogen degradation products (X, Y, D and E) and the A alpha-, B beta- and gamma-chains of fibrinogen. Binding between urinary PCI and fibrin(ogen)-Sepharose was slightly suppressed (16%) by alpha-methylmannose and largely suppressed (42%) by EACA, which indicates that the carbohydrate chain and the lysine binding site participate in the binding. These findings suggest that urinary PCI binds to fibrin(ogen) via the A alpha-, B beta- and gamma-chains and its binding is partly mediated by carbohydrate and the lysine binding site.

Publication types

  • Comparative Study

MeSH terms

  • Aminocaproic Acid / pharmacology
  • Binding Sites / drug effects
  • Fibrin / metabolism*
  • Fibrin Fibrinogen Degradation Products / metabolism
  • Fibrinogen / metabolism*
  • Fibrinolysis
  • Humans
  • Ligands
  • Methylmannosides / pharmacology
  • Plasminogen Inactivators / metabolism*
  • Protein C Inhibitor

Substances

  • Fibrin Fibrinogen Degradation Products
  • Ligands
  • Methylmannosides
  • Plasminogen Inactivators
  • Protein C Inhibitor
  • methylmannoside
  • Fibrin
  • Fibrinogen
  • Aminocaproic Acid