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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...
Formation of the Platelet Plug01:22

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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.
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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...
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

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Introduction to Hemostasis01:05

Introduction to Hemostasis

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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.
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Related Experiment Video

Updated: May 8, 2026

Investigating von Willebrand Factor Pathophysiology Using a Flow Chamber Model of von Willebrand Factor-platelet String Formation
08:30

Investigating von Willebrand Factor Pathophysiology Using a Flow Chamber Model of von Willebrand Factor-platelet String Formation

Published on: August 14, 2017

The interaction between factor H and Von Willebrand factor.

Shuju Feng1, Xiaowen Liang, Miguel A Cruz

  • 1Division of Internal Medicine, Benign Hematology, University of Texas, M. D. Anderson Cancer Center, Houston, Texas, USA.

Plos One
|August 31, 2013
PubMed
Summary

Complement factor H (fH) binds to von Willebrand factor (VWF) and enhances its cleavage by ADAMTS-13. This interaction may influence thrombotic microangiopathy (TMA) pathogenesis, offering new therapeutic targets.

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Last Updated: May 8, 2026

Investigating von Willebrand Factor Pathophysiology Using a Flow Chamber Model of von Willebrand Factor-platelet String Formation
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Area of Science:

  • Biochemistry
  • Hematology
  • Molecular Biology

Background:

  • Complement factor H (fH) regulates the alternative complement pathway, and its mutations are linked to atypical hemolytic uremic syndrome (aHUS).
  • Thrombotic thrombocytopenic purpura (TTP), a common thrombotic microangiopathy (TMA), results from deficient ADAMTS-13 activity on von Willebrand factor (VWF).

Purpose of the Study:

  • To investigate the potential interaction between fH and VWF.
  • To determine if fH influences ADAMTS-13-mediated VWF cleavage.

Main Methods:

  • Co-immunoprecipitation (co-IP) and surface plasmon resonance assays to detect fH-VWF binding.
  • Western-blotting, fluorometric assays (FRETS-VWF73), and flow-based assays to assess VWF cleavage.
  • Utilized recombinant full-length and truncated fH molecules.

Main Results:

  • Factor H directly binds to VWF in plasma and in purified forms, including VWF A1 and A2 domains.
  • Factor H significantly enhances ADAMTS-13-mediated cleavage of VWF, particularly the A2 domain.
  • The C-terminal half of fH is crucial for VWF-A2 binding and ADAMTS-13-mediated cleavage enhancement.

Conclusions:

  • Factor H interacts with VWF.
  • Factor H modulates VWF cleavage by ADAMTS-13, suggesting a role in TMA pathophysiology.