Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

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...
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...
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...
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.

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Protein disulfide isomerase regulation by nitric oxide maintains vascular quiescence and controls thrombus formation.

Journal of thrombosis and haemostasis : JTH·2018
Same author

Novel assay demonstrates that coronary artery disease patients have heightened procoagulant platelet response.

Journal of thrombosis and haemostasis : JTH·2018
Same author

Evaluation of chromogenic factor IX assays by automated protocols.

Haemophilia : the official journal of the World Federation of Hemophilia·2018
Same author

Laboratory monitoring issues in recombinant porcine FVIII replacement in acquired haemophilia A.

Haemophilia : the official journal of the World Federation of Hemophilia·2018
Same author

Optical imaging of cell death in traumatic brain injury using a heat shock protein-90 alkylator.

Cell death & disease·2013
Same author

Pharmaceutical development of the novel arsenical based cancer therapeutic GSAO for Phase I clinical trial.

International journal of pharmaceutics·2012

Related Experiment Video

Updated: May 10, 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

Encryption and decryption of tissue factor.

V M Chen1, P J Hogg

  • 1Lowy Cancer Research Centre and Prince of Wales Clinical School, University of New South Wales, Sydney, NSW, Australia.

Journal of Thrombosis and Haemostasis : JTH
|July 2, 2013
PubMed
Summary
This summary is machine-generated.

Tissue factor (TF) regulates blood clotting and thrombus formation. Its decryption on myeloid cells involves a dithiol/disulfide switch, potentially mediated by protein disulfide isomerase, but the exact mechanism requires further investigation.

Keywords:
allosteric disulfide bondcoagulationdecryptionencryptionthrombosistissue factor

More Related Videos

Extracellular Vesicle Tissue Factor Activity Assay
03:53

Extracellular Vesicle Tissue Factor Activity Assay

Published on: December 29, 2023

Helical Organization of Blood Coagulation Factor VIII on Lipid Nanotubes
12:24

Helical Organization of Blood Coagulation Factor VIII on Lipid Nanotubes

Published on: June 3, 2014

Related Experiment Videos

Last Updated: May 10, 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

Published on: December 29, 2023

Helical Organization of Blood Coagulation Factor VIII on Lipid Nanotubes
12:24

Helical Organization of Blood Coagulation Factor VIII on Lipid Nanotubes

Published on: June 3, 2014

Area of Science:

  • Biochemistry
  • Hematology
  • Cell Biology

Background:

  • Tissue factor (TF) is a key initiator of blood coagulation, binding and activating factor VIIa (FVIIa).
  • The TF/FVIIa complex generates thrombin, crucial for stable thrombus formation.
  • TF exists in both extravascular and intravascular compartments, with distinct regulatory mechanisms.

Purpose of the Study:

  • To investigate the mechanisms regulating intravascular TF activity, particularly its decryption on leucocytes.
  • To explore the role of dithiol/disulfide bonds and phosphatidylserine exposure in TF decryption.
  • To examine the involvement of purinergic receptors, complement activation, and protein disulfide isomerase in TF decryption.

Main Methods:

  • Review of experimental observations on TF decryption.
  • Analysis of the proposed dithiol/disulfide switch involving the Cys186-Cys209 bond in TF.
  • Examination of studies implicating purinergic receptors, complement, and protein disulfide isomerase in TF regulation.

Main Results:

  • Intravascular TF primarily originates from leucocytes (monocytes/neutrophils) and exists in a cryptic, non-coagulant form.
  • Acute events trigger local TF decryption and subsequent FX activation.
  • Decryption involves a dithiol/disulfide switch and phosphatidylserine exposure, with protein disulfide isomerase implicated.

Conclusions:

  • TF decryption on myeloid cells is linked to purinergic receptor or complement activation.
  • A dithiol/disulfide switch, potentially involving protein disulfide isomerase, is central to TF decryption.
  • The precise molecular mechanism of protein disulfide isomerase in TF encryption/decryption remains to be elucidated.