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

Arachidonate transfer between platelets and lipoproteins.

I I Surya1, G Gorter, J W Akkerman

  • 1Department of Haematology, University Hospital Utrecht, The Netherlands.

Thrombosis and Haemostasis
|December 7, 1992
PubMed
Summary

Lipoproteins like LDL and HDL do not modulate platelet function through receptors. Instead, lipid exchange processes cause arachidonic acid depletion, impairing platelet aggregation and secretion.

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

Reactome - a curated knowledgebase of biological pathways: megakaryocytes and platelets.

Journal of thrombosis and haemostasis : JTH·2012
Same author

The phospholipid composition and cholesterol content of platelet-derived microparticles: a comparison with platelet membrane fractions.

Journal of thrombosis and haemostasis : JTH·2005
Same author

Adhesive surface determines raft composition in platelets adhered under flow.

Journal of thrombosis and haemostasis : JTH·2005
Same author

Involvement of the beta3 E749ATSTFTN756 region in stabilizing integrin alphaIIbbeta3-ligand interaction.

Journal of thrombosis and haemostasis : JTH·2003
Same author

Concentration of rafts in platelet filopodia correlates with recruitment of c-Src and CD63 to these domains.

Journal of thrombosis and haemostasis : JTH·2003
Same author

Platelet activation by the apoB/E receptor-binding domain of LDL.

Thrombosis and haemostasis·2002

Area of Science:

  • Biochemistry
  • Hematology
  • Lipid Metabolism

Background:

  • Platelets possess binding sites for LDL and HDL, but their role in modulating platelet function is unclear.
  • The interaction between platelets and lipoproteins, specifically low-density lipoprotein (LDL) and high-density lipoprotein (HDL), requires further investigation regarding receptor-mediated mechanisms.

Purpose of the Study:

  • To investigate the interaction between human platelets and lipoproteins (LDL and HDL) during prolonged incubation.
  • To determine if lipoproteins modulate platelet functions via receptor-mediated processes or lipid exchange.

Main Methods:

  • Incubation of [3H]arachidonate-labeled human platelets with LDL and HDL for 4 hours.
  • Analysis of [3H]radioactivity transfer to lipoproteins.

Related Experiment Videos

  • Assessment of platelet aggregation, secretion, and thromboxane B2 formation after stimulation.
  • Evaluation of the effect of indomethacin on platelet function.

    • Main Results:

    • Significant transfer of [3H]arachidonate from platelets to LDL and HDL, indicating lipid exchange.
    • Impaired platelet aggregation, secretion, and thromboxane B2 formation due to arachidonic acid depletion.
    • LDL initiated arachidonate metabolism and secretion independent of specific binding sites.
    • Platelet secretion was largely preserved even when prostaglandin synthesis was inhibited.

    Conclusions:

    • Findings suggest lipid exchange, not receptor-mediated processes, is the primary mechanism for platelet-lipoprotein interaction.
    • Arachidonic acid depletion from platelets by lipoproteins impairs platelet function.
    • The study challenges the role of LDL and HDL receptors in modulating platelet activity.