Fibrin Formation: The Role of the Fibrinogen-Fibrin Monomer Complex

Abstract

SummaryThe process of fibrin formation using highly purified fibrinogen and thrombin was studied using laser fluctuation spectroscopy, a method that rapidly determines particle size in a solution. Two periods in fibrin clot formation were noted: an induction period during which no fibrin polymerization occurred and a period of rapid increase in particle size. Direct measurement of fibrin monomer polymerization and fibrinopeptide release showed no evidence of an induction period. These observations were best explained by a kinetic model for fibrin clot formation incorporating a reversible fibrinogen-fibrin monomer complex. In this model, the complex serves as a buffer system during the earliest phase of fibrin formation. This prevents the accumulation of free polymerizable fibrin monomer until an appreciable amount of fibrinogen has reacted with thrombin, at which point the fibrin monomer level rises rapidly and polymerization proceeds. Clinically, the complex may be a homeostatic mechanism preventing pathological clotting during periods of elevated fibrinogen.

Kinetics of the interaction of desAABB–fibrin monomer with immobilized fibrinogen

“…Indeed, when FMs are produced in blood, they form a 1:2 complex with fibrinogen or its derivatives (e.g., complex consisting of one FM and two fibrinogen molecules) 14 ( Figure 2B and C) and exist as soluble stable complexes circulating in plasma, named soluble fibrin (SF). [15][16][17] Therefore, the formation of this stable complex provides a pathway for the solubilization of fibrin monomers produced in circulating blood. Moreover, SF serves as an important marker for the diagnosis and the monitoring of thrombotic diseases such as myocardial infarction, liver cirrhosis, malignant hypercoagulable status, and disseminated intravascular coagulation (DIC).…”

Plasma Soluble Fibrin Monomer Complex as a Marker of Coronary Thrombotic Events in Patients with Acute Myocardial Infarction

“…It generally forms a complex with fibrinogen after releasing fibrinopeptide A and/or fibrinopeptide B, which is termed soluble fibrin (SF) or soluble fibrin monomer complex (FMC). These complexes are found at a high concentration in hypercoagulable state blood (Brass et al 1976;Greff et al 1979). When a cross-linking reaction is induced by activated factor XIII (XIIIa), FMC or SF is converted to insoluble fibrin and forms thrombus (Folk and Finlayson 1977).…”

Suitability of low-molecular-weight heparin(oid)s and a pentasaccharide for an in vitro human thrombosis model.

“…This must indicate that some fibrinogen had been deposited on the coverslip as well, arguing in favor of the formation of fibrinogen-fibrin complexes. 30 There is some evidence that the relatively high concentrations of glycosaminoglycans used for these experiments may cause the formation of such fibrinogen-fibrin complexes. 31 -32 In the present study we have compared the effect of various glycosaminoglycans on platelet deposition, thrombus formation, and fibrin deposition under flow conditions in the in vitro thrombosis model.…”