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Related Concept Videos

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...
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...
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.
Coagulation01:09

Coagulation

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...
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...

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Related Experiment Video

Updated: Jul 2, 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

Tissue factor storage, synthesis and function in normal and activated human platelets.

Diego Mezzano1, Valeria Matus, Claudia G Sáez

  • 1Department of Hematology-Oncology, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile. dmezzano@med.puc.cl

Thrombosis Research
|August 12, 2008
PubMed
Summary

The origin of blood-borne tissue factor (TF) in platelets is debated. Research suggests platelets may contain preformed TF, impacting hemostasis and thrombus formation models.

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

Published on: February 14, 2017

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Last Updated: Jul 2, 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

Extracellular Vesicle Tissue Factor Activity Assay
03:53

Extracellular Vesicle Tissue Factor Activity Assay

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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

Area of Science:

  • Hematology
  • Biochemistry
  • Cell Biology

Background:

  • The source and role of blood-borne tissue factor (TF) in hemostasis are controversial.
  • Platelet TF presence was previously attributed to external transfer, but recent studies suggest de novo synthesis.

Purpose of the Study:

  • To investigate the presence and functional significance of tissue factor (TF) within human platelets.
  • To clarify whether platelets contain preformed TF or synthesize it upon activation.

Main Methods:

  • Review of recent literature on TF expression and activity in platelets.
  • Analysis of studies reporting TF-mRNA, neo-synthesis, and procoagulant activity (PCA) in platelets.

Main Results:

  • Conflicting evidence exists regarding preformed versus newly synthesized TF in platelets.
  • Some studies indicate platelets possess readily functional TF upon activation, while others suggest de novo synthesis is required.

Conclusions:

  • The findings challenge current hemostasis models, suggesting platelets may initiate thrombin generation and clot formation.
  • Further research is essential to validate a platelet-centric model of hemostasis and thrombosis.