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 Experiment Videos

[Platelet--vessel wall interactions].

Dominique Baruch1

  • 1INSERM Unité 765, Paris, France. dominique.baruch@univ-paris5.fr

Therapie
|January 25, 2007
PubMed
Summary
This summary is machine-generated.

Platelet activation, crucial for blood clot formation, relies on von Willebrand factor (VWF) interactions under high shear stress. Deficiencies in ADAMTS13 enzyme lead to ultra-large VWF multimers, causing micro-thrombi and contributing to inflammation.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

F-actin disassembly by the oxidoreductase MICAL1 promotes mechano-dependent VWF-GPIbα interaction in platelets.

Nature communications·2025
Same author

Mitochondrial dynamics and reactive oxygen species initiate thrombopoiesis from mature megakaryocytes.

Blood advances·2021
Same author

Role of oculocerebrorenal syndrome of Lowe (OCRL) protein in megakaryocyte maturation, platelet production and functions: a study in patients with Lowe syndrome.

British journal of haematology·2021
Same author

A comparison of haematopoietic stem cells from umbilical cord blood and peripheral blood for platelet production in a microfluidic device.

Vox sanguinis·2019
Same author

LIM kinase/cofilin dysregulation promotes macrothrombocytopenia in severe von Willebrand disease-type 2B.

JCI insight·2016
Same author

A genetically-engineered von Willebrand disease type 2B mouse model displays defects in hemostasis and inflammation.

Scientific reports·2016

Area of Science:

  • Hematology
  • Vascular Biology
  • Biochemistry

Context:

  • The vascular endothelium normally prevents blood clot formation.
  • Platelets are key players in responding to vascular injury, initiating thrombus formation.
  • High shear forces significantly influence platelet behavior and thrombus development.

Purpose:

  • To elucidate the role of von Willebrand factor (VWF) in platelet adhesion and aggregation under varying shear conditions.
  • To explain the mechanism of VWF multimer processing by ADAMTS13 and its implications in thrombotic disorders.
  • To investigate the involvement of platelet-VWF interactions in endothelial cell activation and inflammation.

Summary:

  • Platelet adhesion and thrombus formation are critically dependent on von Willebrand factor (VWF) interactions with platelet receptors glycoprotein Ib (GPIb) and alphaIIbbeta3 integrin, particularly under high shear stress.

Related Experiment Videos

  • Ultra-large VWF multimers, normally cleaved by ADAMTS13, are highly thrombogenic; their accumulation due to ADAMTS13 deficiency leads to micro-thrombi, as observed in thrombotic thrombocytopenic purpura.
  • Platelet-VWF interactions, including VWF and P-selectin release, contribute to leukocyte and platelet adhesion, and activate endothelial cells, thereby promoting inflammation.

    • Impact:

    • Understanding these mechanisms is vital for developing targeted therapies for thrombotic disorders and inflammatory conditions.
    • Highlights the dual role of VWF in both thrombosis and inflammation.
    • Provides insights into the pathophysiology of diseases like thrombotic thrombocytopenic purpura.