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ECPB 2016, 73(1): 74–84
https://doi.org/10.25040/ecpb2016.01.074
Clinical physiology and biochemistry

Mechanisms of the Fibrin Deposits Formation

PETIK A., ANDRIANOVA K., SLOMINSKIY O., ANDRIANOV S.
Abstract

The problem of fibrin and fibrin deposits formation on the inflammation area was reviewed. The data for the system of maintaining the hemostasis balance under normal conditions were summarized and discussed in detail. The evidence of endothelial cells’ defining role in ensuring this balance was provided. The regulatory role of protein C system in thrombin generation level was investigated. The interaction between changes in endothelial cells properties and local enzymatic activity changes of blood plasma due to the inflammatory process was described. The proofs of histamine’s role as a trigger factor for local changes in the status of blood vessels were considered.

Release of histamine leads to the induction of lipid peroxidation. Lipid peroxidation products act as second messengers in inflammatory process. They attract immune cells to the inflammation area by chemotaxis and activate them. Monocytes, in turn, secrete interleukins 1 and 6, tumor necrosis factor alpha. Hydroxyacids that formed as a result of lipid peroxidation modify the physicochemical properties of the lipid bilayer of endotheliocyte’s outer membranes and induce changes in their phenotype via receptor-dependent mechanisms. Interleukin-1 and tumor necrosis factor-α, in turn, induce thrombomodulin internalization, locally decrease protein C system activity and thromboplastin expression. Thus, the properties of endothelial cells turn from thromboresistant to thromboplastic. Simultaneously blood plasma appears saturated by immunocompetent cell vesicles with thromboplastin expressing in their surface. Platelets and polymorphonucleocytes get involved into this process via P-selectin-dependent mechanism. Therefore, the conditions for mass prothrombin activation in the inflammation area and fibrin formation are formed. Besides, endothelial and immunocompetent cells actively release plasminogen activator inhibitors and activate existing inhibitors of fibrinolysis, primarily TAFI. The accumulation of fibrinolytic inhibitors leads to the fibrin polymer’s half-life prolongation and thereby to the extension of fibrin clots destruction. Thus, the local changes in the hemostatic system shift its balance towards the formation of fibrin.

The endothelial phenotype changing escalation under the influence of activated blood coagulation factors, particularly thrombin, was demonstrated. The induction of endothelial cell retraction with endothelial gaps formation and dramatic increasing of the permeability of the blood vessels walls in the inflammation area were described. The accumulation of proteinases and their inhibitors in the inflammation area were thoroughly reviewed. The mechanisms of plasminogen molecule limited proteolysis were described.

Different possible ways of angiostatins formation were outlined. The decelerating role of angiostatins in fibrin clot degradation was shown. Synergetic impact of angiostatins and plasminogen degradation forms on fibrinolysis inhibition was proved. Their impact on processes of fibrinolysis and the fibrin deposits preservation was discussed as well. The inhibition of fibrin degradation in the inflammation area promotes the parietal fibrin deposition with subsequent stable fibrin deposits formation. Thus, inflammatory cytokines promote endothelial cell phenotype turns from thromboresistant to thromboplastic. Also they activate procoagulant activity of immune cells. Consequently, shifting of hemostatic system balance towards the fibrin formation and deposition is the physiological nature of the inflammatory process.

Keywords: inflammation, fibrin, endothelial cells, thrombin, plasmin

Full text: PDF (Ukr) 1.55M

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