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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...
Intracellular Signaling Affects Focal Adhesions01:17

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...
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.
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...
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.
The three phases of hemostasis involve many clotting factors present in plasma and several substances released by platelets and injured tissue cells. It is a fast, localized, and...

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Related Experiment Video

Updated: May 27, 2026

Laminar Flow-based Assays to Investigate Leukocyte Recruitment on Cultured Vascular Cells and Adherent Platelets
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Laminar Flow-based Assays to Investigate Leukocyte Recruitment on Cultured Vascular Cells and Adherent Platelets

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Platelet-leukocyte interactions in thrombosis.

Chiara Cerletti1, Chiara Tamburrelli, Benedetta Izzi

  • 1Research Laboratories, Fondazione di Ricerca e Cura Giovanni Paolo II, Università Cattolica, 86100 Campobasso, Italy. ccerletti@rm.unicatt.it

Thrombosis Research
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Platelet-leukocyte aggregates, markers of prothrombotic states, link inflammation and thrombosis in cardiovascular disease. Natural compounds show promise in inhibiting their formation, requiring further human studies.

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Real-time Imaging of Heterotypic Platelet-neutrophil Interactions on the Activated Endothelium During Vascular Inflammation and Thrombus Formation in Live Mice
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Intravital Microscopy of Leukocyte-endothelial and Platelet-leukocyte Interactions in Mesenterial Veins in Mice
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Intravital Microscopy of Leukocyte-endothelial and Platelet-leukocyte Interactions in Mesenterial Veins in Mice

Published on: August 13, 2015

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Last Updated: May 27, 2026

Laminar Flow-based Assays to Investigate Leukocyte Recruitment on Cultured Vascular Cells and Adherent Platelets
08:50

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Published on: April 9, 2018

Real-time Imaging of Heterotypic Platelet-neutrophil Interactions on the Activated Endothelium During Vascular Inflammation and Thrombus Formation in Live Mice
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Real-time Imaging of Heterotypic Platelet-neutrophil Interactions on the Activated Endothelium During Vascular Inflammation and Thrombus Formation in Live Mice

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Intravital Microscopy of Leukocyte-endothelial and Platelet-leukocyte Interactions in Mesenterial Veins in Mice
05:12

Intravital Microscopy of Leukocyte-endothelial and Platelet-leukocyte Interactions in Mesenterial Veins in Mice

Published on: August 13, 2015

Area of Science:

  • Cardiovascular Biology
  • Hematology
  • Immunology

Background:

  • Activated platelets interact with leukocytes, forming circulating mixed aggregates.
  • These aggregates are reliable markers of a prothrombotic state linked to cardiovascular conditions.
  • Platelet P-selectin and leukocyte P-selectin glycoprotein ligand-1 (PSGL-1) are key mediators of this interaction.

Purpose of the Study:

  • To review the determinants of platelet-leukocyte aggregate formation.
  • To discuss associated pathological conditions and heritability.
  • To explore natural compounds as potential inhibitors of aggregate formation.

Main Methods:

  • Review of literature on platelet-leukocyte interactions.
  • Analysis of molecular mechanisms involving P-selectin and PSGL-1.
  • Examination of in vitro and animal model studies on natural compound effects.

Main Results:

  • Platelet-leukocyte aggregate formation involves P-selectin/PSGL-1 signaling, leading to Mac-1 activation and firm adhesion.
  • Aggregate formation upregulates leukocyte tissue factor and inflammatory cytokines, promoting thrombotic progression.
  • Natural compounds like polyphenols show inhibitory effects in preclinical studies.

Conclusions:

  • Platelet-leukocyte aggregates bridge inflammation and thrombosis in atherogenesis.
  • Understanding these interactions is crucial for preventing and treating ischemic cardiovascular disease.
  • Further human trials are needed to validate the efficacy of natural compounds.