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Related Concept Videos

Formation of the Platelet Plug01:22

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...
Structure and Function of Platelets01:18

Structure and Function of Platelets

The cell fragments known as platelets are disc-shaped, with an average diameter of about 3 μm and a thickness of roughly 1 μm. They play a crucial role in the body's vascular clotting system, which also involves plasma proteins, blood cells, and blood vessel tissues.
Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000 platelets, with...
Extrinsic and Intrinsic Pathways of Hemostasis01:20

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...
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

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...
Clot Retraction and Fibrinolysis01:16

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.
Introduction to Hemostasis01:05

Introduction 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.
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Related Experiment Video

Updated: May 11, 2026

Flow Cytometry Analysis of Tissue Factor Expression in Human Platelets
10:08

Flow Cytometry Analysis of Tissue Factor Expression in Human Platelets

Published on: November 22, 2024

Human platelets do not express tissue factor.

Bjarne Østerud1, Jan Ole Olsen

  • 1Department of Medical Biology, Faculty of Health Sciences, University of Tromsø, 9037 Tromsø, Norway. bjarne@fagmed.uit.no

Thrombosis Research
|April 30, 2013
PubMed
Summary

Platelets do not express tissue factor (TF) activity after stimulation. Monocyte contamination, not platelet de novo synthesis, explains previously observed TF activity, refuting a role for Toll-like receptor 4.

Keywords:
ComplementFVFVIIaFX/FXaFactor VFactor VIIaFactor X/Factor XaIgGLPSMonocytesP-selectin glycoprotein ligand-1PCAPMAPRPPSPSGL-1PlateletsTFTFPITLR4TRAPTissue factorimmunoglobulinlipopolysaccharidephorbol myristate acetatephosphatidylserineplatelet rich plasmaprocoagulant activitythrombin receptor-activating peptidetissue factortissue factor pathway inhibitortoll like receptor 4

More Related Videos

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time
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

Extracellular Vesicle Tissue Factor Activity Assay
03:53

Extracellular Vesicle Tissue Factor Activity Assay

Published on: December 29, 2023

Related Experiment Videos

Last Updated: May 11, 2026

Flow Cytometry Analysis of Tissue Factor Expression in Human Platelets
10:08

Flow Cytometry Analysis of Tissue Factor Expression in Human Platelets

Published on: November 22, 2024

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time
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

Extracellular Vesicle Tissue Factor Activity Assay
03:53

Extracellular Vesicle Tissue Factor Activity Assay

Published on: December 29, 2023

Area of Science:

  • Hematology
  • Immunology
  • Cell Biology

Background:

  • Controversy exists regarding de novo synthesis of tissue factor (TF) in platelets.
  • Platelet isolation methods, assays, and reagents, including non-specific antibodies, may contribute to observed TF expression diversity.
  • This study investigates TF expression potential in purified human platelets using a sensitive and specific TF activity assay.

Purpose of the Study:

  • To evaluate the potential for de novo tissue factor (TF) synthesis in human platelets.
  • To clarify the role of monocytes in observed platelet TF activity.
  • To investigate the involvement of Toll-like receptor 4 (TLR4) in platelet TF expression.

Main Methods:

  • Human platelets were isolated and anti-coagulated.
  • Platelets were stimulated with lipopolysaccharide (LPS) plus phorbol 12-myristate 13-acetate (PMA), IgG antibody, or thrombin receptor-activating peptide (TRAP).
  • TF activity was measured using a highly specific assay, with and without immune-adsorption to remove monocytes.

Main Results:

  • LPS/PMA stimulation resulted in trace TF-like activity (PCA) not inhibited by anti-TF antibody.
  • Platelets without monocyte removal showed significant TF activity, abolished by anti-TF antibody, indicating monocyte-derived TF.
  • TRAP activation and IgG antibody stimulation yielded only trace PCA, with no evidence of TF activity mediated by complement activation.

Conclusions:

  • Monocyte-free platelets do not express TF activity upon stimulation with LPS or activated complement factors.
  • This finding suggests no role for Toll-like receptor 4 (TLR4) in platelet TF expression.
  • No evidence supports TF activity associated with platelets from rapid, dynamic processes.