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Related Concept Videos

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...
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.
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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.
Phosphoinositides and PIPs01:42

Phosphoinositides and PIPs

Phosphoinositides are a group of phospholipids containing a glycerol backbone with two fatty acid chains and a phosphate attached to a myoinositol sugar ring. The inositol head group extends into the cytoplasm, where it is modified by adding phosphate groups to form phosphatidylinositol phosphates or PIPs.
Different phosphoinositides are synthesized and recruited on the cytosolic face of the plasma membrane. The localization of specific phosphoinositides concentrated in separate membrane...

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Related Experiment Video

Updated: Jun 23, 2026

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
04:37

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation

Published on: May 23, 2025

Two distinct pathways regulate platelet phosphatidylserine exposure and procoagulant function.

Simone M Schoenwaelder1, Yuping Yuan, Emma C Josefsson

  • 1Australian Centre for Blood Diseases, Monash University, 89 Commercial Road, Melbourne, Victoria 3004, Australia.

Blood
|April 24, 2009
PubMed
Summary

Platelets have two distinct pathways regulating their procoagulant function. Apoptosis induction via ABT-737 activates a Bak/Bax- and caspase-dependent pathway, while platelet activation uses a calcium-dependent pathway.

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Analyzing Platelet Subpopulations by Multi-color Flow Cytometry
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Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
04:37

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Published on: May 23, 2025

Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets
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Analyzing Platelet Subpopulations by Multi-color Flow Cytometry
08:04

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Published on: June 10, 2025

Area of Science:

  • Hematology
  • Cell Biology
  • Biochemistry

Background:

  • Procoagulant platelets share features with apoptotic cells, such as phosphatidylserine (PS) exposure.
  • The role of apoptosis regulators in platelet procoagulant function remains largely unknown.

Purpose of the Study:

  • To investigate the distinct pathways regulating platelet procoagulant function.
  • To determine the role of Bak, Bax, and caspases in apoptosis-induced procoagulant activity.
  • To compare apoptosis-mediated procoagulant function with activation-induced procoagulant function.

Main Methods:

  • Platelets were treated with the BH3 mimetic ABT-737 to induce apoptosis.
  • The role of Bak and Bax was assessed using knockout platelets (Bak(-/-)Bax(-/-)).
  • Caspase activity was inhibited, and platelet activation inhibitors and calcium chelators were used.

Main Results:

  • ABT-737 treatment induced PS exposure and increased thrombin generation in a Bak/Bax- and caspase-dependent manner.
  • This apoptosis-induced procoagulant function was independent of platelet activation pathways and extracellular calcium.
  • Agonist-induced procoagulant function was unaffected by Bak/Bax deficiency or caspase inhibition but was abolished by calcium chelation and activation inhibitors.

Conclusions:

  • Two distinct pathways regulate platelet procoagulant function: one linked to apoptosis (Bak/Bax/caspase-dependent) and another to platelet activation (calcium/activation-dependent).
  • Understanding these pathways is crucial for comprehending hemostasis and thrombosis.