Related Experiment Video
Updated: Jun 28, 2026

03:53
Extracellular Vesicle Tissue Factor Activity Assay
Published on: December 29, 2023
Plasmin enhances cell surface tissue factor activity in mesothelial and endothelial cells
1Biomedical Research, The University of Texas Health Science Center, Tyler, TX 75708, USA.
Journal of Thrombosis and Haemostasis : JTH
|November 6, 2008
Summary
Thrombin increases tissue factor (TF) in mesothelial cells via gene activation, while plasmin enhances TF activity by degrading TFPI. This clarifies protease roles in pleural injury responses.
Area of Science:
- Cell Biology
- Hemostasis and Thrombosis
- Protease-activated Signaling
Background:
- Mesothelial cells regulate local coagulation and fibrinolysis.
- Mechanisms of increased tissue factor (TF) expression in mesothelial cells post-injury are not fully understood.
Purpose of the Study:
- To determine if plasmin or thrombin induce TF expression in human pleural mesothelial cells (HMC).
- To elucidate the molecular mechanisms underlying protease-induced TF expression in HMC.
Main Methods:
- HMC and HUVEC exposed to plasmin or thrombin.
- TF activity measured via Factor Xa generation assay.
- TF antigen and mRNA levels analyzed by immunoblot and Northern blot.
Main Results:
- Both plasmin and thrombin increased HMC TF activity 3-4 fold.
- Thrombin induced de novo TF synthesis; plasmin did not.
- Plasmin inactivated cell-associated TFPI through proteolysis.
Conclusions:
- Thrombin up-regulates TF activity in HMC via transcriptional activation.
- Plasmin increases TF activity by proteolytically inactivating cell-associated TFPI.
More Related Videos
Related Concept Videos
Clot 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.
Intracellular Signaling Affects Focal Adhesions
Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
Some...
Extrinsic 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...
Formation 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...
Cytoskeletal Linker Proteins - Plakins
Plakins are large proteins with binding domains for microtubules, microfilaments, intermediate filaments, and membrane-associated protein complexes at cell junctions. Plakin functions are evolutionarily conserved and are primarily involved in organizing the different components of the cytoskeleton by crosslinking them to each other and connecting them to the cell-matrix and cell adhesion complexes. They are also known to interact with signal transducers, serve as scaffolds for signaling...
Anticoagulant 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...

