Related Experiment Video
Updated: Aug 11, 2026
07:09
Experimental and Imaging Techniques for Examining Fibrin Clot Structures in Normal and Diseased States
Published on: April 1, 2015
Soluble fibrin species in arterial thrombi
G Sandbaek1, S Bjørnsen, J H Sobel
1Research Institute for Internal Medicine, The National Hospital (Rikshospitalet), University of Oslo, Norway. gunnar.sandbaek@rh.uio.no
Summary
This study identified cross-linked fibrin derivatives in soluble arterial thrombi, indicating active clot breakdown. These findings support a dynamic balance between blood clot formation and lysis.
Area of Science:
- Biochemistry
- Hematology
- Molecular Biology
Background:
- Fibrin(ogen) species within human arterial thrombi are not fully characterized.
- Understanding thrombus composition is crucial for developing effective thrombolytic therapies.
Purpose of the Study:
- To characterize soluble fibrin(ogen) species in human arterial thrombi.
- To investigate the degradation state of fibrin and fibrinogen within thrombi.
Main Methods:
- Immunoblotting technique applied to supernatant from arterial thrombi.
- Polyacrylamide gel electrophoresis (PAGE) of reduced and unreduced samples.
- Use of specific anti-fibrin(ogen) antibodies.
Main Results:
- Detected high molecular weight alpha-chain polymers and gammagamma-dimers.
- Identified lower molecular weight chains (alpha, beta, gamma).
- Found no intact fibrinogen; des-AABB fibrin was a major soluble derivative with C-terminally degraded alpha-chains.
Conclusions:
- Demonstrated cross-linked fibrin derivatives in soluble arterial thrombus material.
- Fibrin derivatives were C-terminally degraded X-oligomers, likely from plasmin degradation.
- Results support a dynamic equilibrium between clotting and lysis in thrombi.
Related Concept Videos
01:30Anticoagulant Drugs: Low-Molecular-Weight Heparins
Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
01:05Introduction to Hemostasis
Hemostasis is a complex physiological process that prevents excessive bleeding when a blood vessel is injured. It's crucial for maintaining the integrity of the circulatory system, as it ensures that our blood remains fluid while still within the vascular network and yet clots to prevent blood loss upon vessel injury.
The three phases of hemostasis involve many clotting factors present in plasma and several substances released by platelets and injured tissue cells. It is a fast, localized, and...
The three phases of hemostasis involve many clotting factors present in plasma and several substances released by platelets and injured tissue cells. It is a fast, localized, and...
01:22Formation of the Platelet Plug
The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
01:20Extrinsic and Intrinsic Pathways of Hemostasis
Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which forms a...
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which forms a...
01:16Clot Retraction and Fibrinolysis
After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
01:30Venous Thrombosis I: Introduction
Venous thrombosis, the most common disorder of the veins, involves the formation of a thrombus or blood clot associated with vein inflammation. It can be classified as either superficial vein thrombosis or deep vein thrombosis.Superficial Vein Thrombosis: This involves the formation of a thrombus in a superficial vein, usually the greater or lesser saphenous vein. Though less severe than deep vein thrombosis (DVT), SVT can lead to complications if untreated.Deep Vein Thrombosis (DVT): This...