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

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.
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...
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...
Fibronectins Connect Cells with ECM01:25

Fibronectins Connect Cells with ECM

Fibronectin is an adhesive glycoprotein present in the extracellular matrix of embryogenic and adult tissue. These molecules primarily aid in regulating cell motility and attachment. A fibronectin molecule is composed of two identical polypeptide chains attached to each other by a pair of disulfide bonds at the C-terminal.
Both proteoglycans and collagen are attached to fibronectin proteins, which, in turn, are attached to integrin proteins. These integrin proteins interact with transmembrane...
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 Higher-order Actin Filaments01:11

Formation of Higher-order Actin Filaments

The polymerization of G-actin monomers into filamentous F-actin is a multi-step process. Once the F-actins are formed, they can bundle together in different arrangements to form higher-order networks and regulate cellular functions. Common examples include the formation of lamellipodia and filopodia at the cell's leading edge by actin reorganization in a migrating cell. The microvilli on the brush border epithelial cells are also formed through the F-actin network.
The high-order actin networks...

You might also read

Related Articles

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

Sort by
Same author

cGAS/STING is associated with brain-gut-liver axis disturbance and systemic inflammation in cerebral ischemia.

Biochemical and biophysical research communications·2026
Same author

Epigenetic Perspectives on Maternal Gut Microbiota's Impact on Embryonic and Fetal Development.

Comprehensive Physiology·2026
Same author

Ginkgo biloba extract suppresses hepatocellular carcinoma progression by inhibiting the recruitment of myeloid-derived suppressor cells through reduced CXCL1 secretion via SRC downregulation.

Frontiers in immunology·2026
Same author

Engineered VPg saRNA achieves cap-independent, low-immunogenic and precise encoding of therapeutic proteins in vivo.

Nature communications·2026
Same author

Tmem110 regulates the conformation of TRPML1 to maintain endolysosomal homeostasis and prevent mitochondrial DNA leakage and pathological self-DNA processing.

Nature communications·2026
Same author

A bibliometric analysis of 2000-2024 on interventional therapy for liver cancer and tumor immune microenvironment.

Chinese clinical oncology·2026

Related Experiment Video

Updated: May 10, 2026

Experimental and Imaging Techniques for Examining Fibrin Clot Structures in Normal and Diseased States
07:09

Experimental and Imaging Techniques for Examining Fibrin Clot Structures in Normal and Diseased States

Published on: April 1, 2015

Fibrin networks regulate protein transport during thrombus development.

Oleg V Kim1, Zhiliang Xu, Elliot D Rosen

  • 1Department of Applied and Computational Mathematics and Statistics, University of Notre Dame, South Bend, Indiana, United States of America.

Plos Computational Biology
|June 21, 2013
PubMed
Summary

A novel fibrin cap mechanism limits thrombus growth by regulating protein transport. This finding reveals how fibrin caps prevent small thrombi from becoming life-threatening events.

More Related Videos

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

Analysis of β-Amyloid-induced Abnormalities on Fibrin Clot Structure by Spectroscopy and Scanning Electron Microscopy
06:27

Analysis of β-Amyloid-induced Abnormalities on Fibrin Clot Structure by Spectroscopy and Scanning Electron Microscopy

Published on: November 30, 2018

Related Experiment Videos

Last Updated: May 10, 2026

Experimental and Imaging Techniques for Examining Fibrin Clot Structures in Normal and Diseased States
07:09

Experimental and Imaging Techniques for Examining Fibrin Clot Structures in Normal and Diseased States

Published on: April 1, 2015

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

Analysis of β-Amyloid-induced Abnormalities on Fibrin Clot Structure by Spectroscopy and Scanning Electron Microscopy
06:27

Analysis of β-Amyloid-induced Abnormalities on Fibrin Clot Structure by Spectroscopy and Scanning Electron Microscopy

Published on: November 30, 2018

Area of Science:

  • Biophysics
  • Hematology
  • Biomedical Engineering

Background:

  • Thromboembolic disease poses a significant global health burden.
  • Understanding mechanisms that inhibit thrombus growth is crucial for developing new treatments.
  • Previous research indicated stabilized thrombi are covered by a fibrin network.

Purpose of the Study:

  • To investigate the role of the fibrin cap in regulating thrombus growth.
  • To elucidate the mechanism of protein transport through the fibrin network of a thrombus.
  • To determine how the fibrin cap limits platelet activation and thrombus expansion.

Main Methods:

  • Integration of experimental studies with computational model simulations.
  • Experiments conducted in microfluidic devices to study protein transport through fibrin networks.
  • In vivo studies in mice to observe fibrin cap formation on non-occluding thrombi.

Main Results:

  • Network permeability and protein diffusivity are key factors in fibrin network transport.
  • Model simulations demonstrated thrombin is washed out via the fibrin network, reducing platelet exposure.
  • The fibrin cap restricts platelet access to high thrombin concentrations, limiting activation and growth.

Conclusions:

  • The fibrin cap acts as a critical regulator of thrombus growth by controlling protein diffusion and platelet activation.
  • This mechanism prevents the progression of small, non-occluding thrombi into dangerous thromboembolic events.
  • Findings offer insights into potential therapeutic strategies targeting thrombus formation and progression.