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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...
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.
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...
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...
Vascular Spasm01:16

Vascular Spasm

The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last for...

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Related Experiment Video

Updated: Jul 11, 2026

Implantation of Fibrin Gel on Mouse Lung to Study Lung-specific Angiogenesis
07:52

Implantation of Fibrin Gel on Mouse Lung to Study Lung-specific Angiogenesis

Published on: December 21, 2014

Fibrinogen induces endothelial cell permeability.

Neetu Tyagi1, Andrew M Roberts, William L Dean

  • 1Department of Physiology and Biophysics, Health Sciences Center, A-1115, University of Louisville, Louisville, KY 40292, USA.

Molecular and Cellular Biochemistry
|September 13, 2007
PubMed
Summary

Elevated fibrinogen (Fg) increases blood vessel permeability by activating endothelial cells. This process, involving ERK signaling and F-actin formation, may contribute to microvascular leakage in cardiovascular disorders.

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Last Updated: Jul 11, 2026

Implantation of Fibrin Gel on Mouse Lung to Study Lung-specific Angiogenesis
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Study of the Actin Cytoskeleton in Live Endothelial Cells Expressing GFP-Actin
08:37

Study of the Actin Cytoskeleton in Live Endothelial Cells Expressing GFP-Actin

Published on: November 18, 2011

Area of Science:

  • Biochemistry
  • Cell Biology
  • Physiology

Background:

  • Increased fibrinogen (Fg) levels are observed in cardiovascular and cerebrovascular disorders.
  • Fg and its degradation products are linked to inflammation and microvascular leakage.

Purpose of the Study:

  • To investigate if high fibrinogen levels increase endothelial cell (EC) permeability.
  • To determine the role of extracellular signal regulated kinase (ERK) signaling and F-actin formation in this process.

Main Methods:

  • Cultured endothelial cells were treated with fibrinogen.
  • Analyzed ERK phosphorylation, F-actin formation, and EC permeability to albumin.

Main Results:

  • Fg binding to ICAM-1 and α5β1 integrin induced ERK phosphorylation.
  • This led to increased F-actin formation, gap formation between ECs, and enhanced albumin permeability.

Conclusions:

  • Elevated, non-degraded fibrinogen increases EC permeability via ERK signaling and F-actin induction.
  • This mechanism contributes to microvascular leakage in cardiovascular and cerebrovascular diseases.