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The effect of thrombin on the dynamic exchange between intraplatelet and extraplatelet fibrinogen
Author(s) -
Vila Virtudes,
MartínezSales Vicenta,
Réga Edelmiro,
Aznar Justo
Publication year - 1997
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.1997.4383248.x
Subject(s) - fibrinogen , thrombin , platelet , chemistry , fibrin , biochemistry , endocrinology , medicine , immunology
We examined the distribution of platelet fibrinogen and the exchange between intra‐ and extra‐platelet fibrinogen in unstimulated and thrombin‐stimulated platelets. In unstimulated platelets 60% of platelet fibrinogen was found in the soluble platelet fraction and 40% in the insoluble one. In platelets activated with thrombin, changes took place in the distribution of intraplatelet fibrinogen but not in the total fibrinogen content. At 0.5 U/ml of thrombin the fibrin(ogen) content of the insoluble and soluble fractions was approximately 80% and 20%, respectively. When we evaluated how extraplatelet fibrinogen affects the content and distribution of intraplatelet fibrinogen, we found that when unlabelled fibrinogen was added to unstimulated and thrombin‐stimulated platelets the content and distribution of intraplatelet fibrinogen remained unaltered. However, when 125 I‐fibrinogen was added, it was incorporated into unstimulated and thrombin‐stimulated platelets. In unstimulated platelets, 70% of the incorporated 125 I‐fibrinogen was in the soluble fraction and 30% in the insoluble. In thrombin‐stimulated platelets the distribution of the incorporated 125 I‐fibrinogen was 62% and 38% in soluble and insoluble fractions respectively. MoAb to GPIIb–IIIa produced 80% and 60% inhibition of 125 I‐fibrinogen incorporation by unstimulated and thrombin‐stimulated platelets. Our data showed dynamic exchange between intraplatelet and extraplatelet fibrinogen both in unstimulated and thrombin‐stimulated platelets mediated mainly by GPIIb–IIIa.