fibrin

(noun)

An elastic, insoluble, whitish protein produced by the action of thrombin on fibrinogen and forming an interlacing fibrous network in the coagulation of blood.

Related Terms

(noun)

A fibrous protein involved in blood clotting.

Related Terms

Examples of fibrin in the following topics:

  • Adhesions

    • As part of the process, the body deposits fibrin onto injured tissues.
    • The fibrin acts like a glue to seal the injury and builds the fledgling adhesion, said at this point to be fibrinous.
    • In many cases however, the production or activity of these enzymes are compromised because of injury and the fibrinous adhesion persists.
    • Fibrinous adhesions are causes of early postoperative obstruction which settles down within 3–5 days.
    • The majority of fibrinous adhesions will disappear in due course.

  • Fibrinolysis

    • The main enzyme in primary fibrinolysis is plasmin, a proteolytic enzyme that degrades fibrin mesh.
    • Plasminogen cannot cleave fibrin and circulates in the bloodstream.
    • Following fibrin degradation by plasmin, old activated platelets from the platelet plug are phagocytized and destroyed by macrophages.
    • Plasmin operates on a negative feedback process because it is reduced when the fibrin clot is fully degraded.
    • Fibrinolytic drugs include synthesized tissue plasminogen activator and streptokinase, a bacterial enzyme that has degrades fibrin directly.

  • Overview of Hemostasis

    • It takes approximately sixty seconds until the first fibrin strands begin to intersperse among the wound.
    • After several minutes, the platelet plug is completely formed by fibrin.
    • Thrombin facilitates the conversion of a soluble plasma protein called fibrinogen into long, insoluble fibers or threads of the protein, fibrin.
    • Fibrin threads wind around the platelet plug at the damaged area of the blood vessel, forming an interlocking network of fibers and a framework for the clot.
    • This temporary fibrin clot can form in less than a minute and slows blood flow before platelets attach.

  • Platelets and Coagulation Factors

    • When the platelets are activated, they clump together to form a platelet plug (fibrin clot) ( b), releasing their contents.
    • Coagulation factors (clotting factors) are proteins in the blood plasma that respond in a complex cascade to convert fibrinogen, a water-soluble protein present in blood serum, into fibrin, a non-water soluble protein, which strengthens the platelet plug.
    • The platelets collect at a wound site in conjunction with other clotting factors, such as fibrinogen, to form a fibrin clot that prevents blood loss and allows the wound to heal.

  • Coagulation

    • Several components of the coagulation cascade, including both cellular (e.g. platelets) and protein (e.g. fibrin) components, are involved in blood vessel repair.
    • Secondary hemostasis refers to the coagulation cascade, which produces a fibrin mesh to strengthen the platelet plug.
    • Thrombin then  cleaves fibrinogen into fibrin, which forms the mesh that binds to and strengthens the platelet plug, finishing coagulation and thus hemostasis.
    • It also activates more factor V, which later acts as an anticoagulant with inhibitor protein C, and factor XIII, which covalently bonds to fibrin to strengthen its attachment to the platelets.
    • Plasmin: generated by proteolytic cleavage of plasminogen, a potent fibrinolytic that degrades fibrin and destroys clots.

  • Direct Damage

    • Streptococcus pyogenes is associated with strep throat and "flesh-eating disease. " The bacteria produce enzymes which function in disrupting fibrin clots.
    • Fibrin clots will form at sites of injury, in this case, at the site of foreign invasion.
    • The enzymes, capable of digesting fibrin, will open an area within the epithelial cells and promote invasion of the bacteria into the tissues.

  • Platelets

    • Platelets also contain adhesive proteins that allow them to adhere to fibrin mesh and the vascular endothelium, as well as to a microtubule and microfilament skeleton that extends into filaments during platelet activation.
    • The adhesive surface proteins of platelets allow them to accumulate on the fibrin mesh at an injury site to form a platelet plug that clots the blood.
    • During coagulation, they release factors that increase local platelet aggregation (thromboxane A), mediate inflammation (serotonin), and promote blood coagulation through increasing thrombin and fibrin (thromboplastin).

  • Blood Plasma

    • Fibrinogen generates fibrin when activated by the coagulant thrombin, which forms a mesh that clots blood with the assistance of a platelet plug. 
    • Normally, anticoagulants and fibrinolytics in the plasma, such as plasmin and heparin, break up fibrin clots and inactivate thrombin.

  • Platelet Plug Formation

    • The coagulation factors include factor V and VIII, which are involved in the coagulation cascade that converts fibrinogen into fibrin mesh after platelet plug formation.
    • The completed plug will cover the damaged components of the endothelium and will stop blood from flowing out of it, but if the wound is large enough, blood will not coagulate until the fibrin mesh from the coagulation cascade is produced, which strengthens the platelet plug.

  • Clot Retraction and Repair

    • These factors cause the fibrin mesh to contract by forming twists and knots that condense the size of the clot.
    • Following clot retraction, a separate process called fibrinolysis occurs which degrades the fibrin of the clot while macrophages consume the expended platelets, thus preventing possible thromboembolism.