Related Experiment Video
Updated: Jul 30, 2026
09:38
A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time
Published on: February 14, 2017
Tissue factor, the blood, and the arterial wall.
1Division of Thrombosis Research, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA.
Trends in Cardiovascular Medicine
|March 10, 2001
Summary
Leukocytes transfer tissue factor (TF) particles to blood clots, promoting thrombus growth. Inhibiting this transfer offers a new therapeutic strategy for preventing thrombosis in various conditions.
Area of Science:
- Cardiovascular biology
- Hematology
- Immunology
Background:
- Thrombogenic tissue factor (TF) on cell-derived microparticles circulates in patients with acute coronary syndromes.
- Previously, it was shown that leukocytes transfer TF-positive particles to platelet thrombi.
Purpose of the Study:
- To investigate the mechanism of TF transfer from leukocytes to platelet thrombi.
- To explore the therapeutic potential of inhibiting TF transfer and activity.
Main Methods:
- Investigated the interaction between leukocytes, TF-positive microparticles, and platelet thrombi.
- Assessed the role of CD15 in TF transfer.
- Evaluated the effects of inhibiting TF transfer and TF activity.
Main Results:
- Leukocyte-derived TF-positive microparticles contribute to thrombus formation and propagation.
- TF transfer is dependent on the interaction of CD15 and TF with platelet thrombi.
- Inhibition of TF transfer and TF activity demonstrated a potential therapeutic effect.
Conclusions:
- Leukocyte-mediated TF transfer is a critical mechanism in arterial thrombosis, challenging the traditional view of vessel-wall injury.
- Targeting TF transfer and activity presents a novel therapeutic avenue for thrombosis prevention, particularly in TF-related disorders.
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...
01:16Vascular Spasm
The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last for...
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...
01:09Coagulation
The coagulation phase is a critical part of the body's process to prevent blood loss following injury to blood vessels. It involves chemical reactions that form a clot to seal the injured area. The clotting process begins shortly after injury, within 15-20 seconds for severe damage and 1-2 minutes for minor injuries.
During the coagulation phase, clotting factors, or procoagulants, play a vital role in initiating and progressing the coagulation cascade. This cascade is a series of reactions...
During the coagulation phase, clotting factors, or procoagulants, play a vital role in initiating and progressing the coagulation cascade. This cascade is a series of reactions...
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.