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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...
Coagulation01:09

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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...
Coagulation01:06

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Colloidal solids are solid particles suspended in solution. They are usually negatively charged, attracting a compact primary layer of positively charged ions, which attract more counterions to form an electrical double layer. Electrostatic repulsion between the charged double layers prevents the particles from colliding, stabilizing the colloids. These solids are often undesirable because they can contain toxins that are difficult to remove. Coagulation is a technique that helps aggregate and...
Introduction to Hemostasis01:05

Introduction to Hemostasis

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Complement System01:27

Complement System

The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a membrane...
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...

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Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
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The procoagulant and proinflammatory plasma contact system.

Thomas Renné1

  • 1Department of Molecular Medicine and Surgery, Karolinska Institutet, Karolinska University Hospital Solna, Stockholm, Sweden. thomas@renne.net

Seminars in Immunopathology
|August 23, 2011
PubMed
Summary

The plasma contact system initiates blood clotting and inflammation. While its in vitro functions are known, in vivo studies reveal its crucial role in thrombus formation and various diseases.

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Area of Science:

  • Biochemistry
  • Physiology
  • Immunology

Background:

  • The contact system is a plasma protease cascade initiated by coagulation factor XII activation.
  • It triggers both procoagulant and proinflammatory reactions through distinct pathways.
  • While its in vitro biochemistry is understood, in vivo functions are emerging.

Purpose of the Study:

  • To provide an overview of the plasma contact system's role in disease.
  • To highlight its contribution to both health and pathology.
  • To discuss its involvement in occlusive and inflammatory conditions.

Main Methods:

  • Review of data from genetically engineered mouse models.
  • Analysis of in vitro and in vivo studies on contact system function.
  • Examination of molecular triggers and disease associations.

Main Results:

  • Contact system proteases are essential for thrombus formation in vivo.
  • Deficiency impairs thrombus formation but not overall hemostasis.
  • The system is activated by platelet-released polyphosphate and contributes to hereditary angioedema, bacterial infection leakage, and allergic edema.

Conclusions:

  • The contact system plays a critical role in in vivo thrombus formation.
  • Dysregulation of the contact system is implicated in various pathological conditions.
  • Understanding the contact system is vital for addressing occlusive and inflammatory diseases.