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Structural changes in platelet glycoprotein IIb/IIIa by plasmin: determinants and functional consequences

B Pasche1, H Ouimet, S Francis

  • 1Cardiology Divisions, Brigham and Women's Hospital, Boston, MA 02115.

Blood
|January 15, 1994
PubMed

Insights

Plasmin cleaves the platelet fibrinogen receptor, glycoprotein IIb/IIIa (GPIIb/IIIa), in plasma. This modification reduces fibrinogen binding and platelet aggregation, impacting blood clotting mechanisms.

Area of Science:

  • Hematology
  • Biochemistry
  • Molecular Biology

Background:

  • Plasmin is known to affect platelet aggregation.
  • The direct impact of plasmin on the platelet fibrinogen receptor, glycoprotein IIb/IIIa (GPIIb/IIIa), in plasma remains unclear.

Purpose of the Study:

  • To investigate the direct effect of plasmin on platelet GPIIb/IIIa in a plasma environment.
  • To assess the consequences of plasmin treatment on platelet aggregation and fibrinogen binding.

Main Methods:

  • Platelets were incubated with plasmin in platelet-rich plasma.
  • Platelet aggregation, fibrinogen binding, and GPIIb/IIIa structural integrity were measured.
  • Immunoblots and peptide sequencing were used to analyze GPIIb/IIIa cleavage.

Main Results:

  • Plasmin treatment dose-dependently reduced maximal reversible fibrinogen binding and the rate of platelet aggregation.
  • Plasmin cleaved GPIIIa, a subunit of GPIIb/IIIa, at the lys444-pro445 bond.
  • This specific cleavage event was observed only in the presence of plasma fibrinogen.

Conclusions:

  • Plasmin induces a unique proteolytic modification of GPIIb/IIIa in plasma, dependent on fibrinogen binding.
  • This plasmin-mediated cleavage significantly reduces fibrinogen binding and platelet aggregation responses.

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