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

Complement complex C5b-8 induces PGI2 formation in cultured endothelial cells.

N Suttorp, W Seeger, S Zinsky

    The American Journal of Physiology
    |July 1, 1987
    PubMed
    Summary

    The terminal complement sequence C5b-8 triggers prostacyclin (PGI2) release in endothelial cells via calcium influx, independent of cell damage. This suggests a novel role for complement in regulating vascular function.

    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

    Shift in bacterial etiology from the CAPNETZ cohort in patients with community-acquired pneumonia: data over more than a decade.

    Infection·2021
    Same author

    [Acute Respiratory Failure after Silicone Injection].

    Pneumologie (Stuttgart, Germany)·2019
    Same author

    Spleen tyrosine kinase inhibition blocks airway constriction and protects from Th2-induced airway inflammation and remodeling.

    Allergy·2016
    Same author

    Drug research·2016
    Same author

    [New Pathogenetic Concepts and Pharmacological Studies on Adjuvant Therapy in Severe Pneumonia].

    Pneumologie (Stuttgart, Germany)·2015
    Same author

    [Smoking: Cardiovascular effects and abstinence strategies].

    Der Internist·2015

    Area of Science:

    • Immunology
    • Cell Biology
    • Vascular Physiology

    Background:

    • The terminal complement sequence plays a role in immune responses and inflammation.
    • Prostacyclin (PGI2) is a key mediator of vascular function, including vasodilation and inhibition of platelet aggregation.
    • Antibody-sensitized pulmonary arterial endothelial cells are implicated in various vascular pathologies.

    Purpose of the Study:

    • To investigate the effect of the terminal complement sequence on prostacyclin (PGI2) generation in pulmonary arterial endothelial cells.
    • To elucidate the role of extracellular calcium and specific complement components in PGI2 release.
    • To explore the mechanism by which complement activation influences endothelial cell function.

    Main Methods:

    • Utilized antibody-sensitized pulmonary arterial endothelial cells.

    Related Experiment Videos

  • Examined PGI2 generation upon exposure to complement complexes (C5b-7, C5b-8, C5b-9).
  • Assessed the role of extracellular calcium, calcium channel blockers, and calmodulin inhibitors (W7, trifluoperazine) on PGI2 release.
  • Measured the influx of 45Ca2+ and other molecules (51Cr O4(2-), [3H] aminobutyric acid, [3H]sucrose, [3H]inulin, [3H]dextran) into cells.

    • Main Results:

    • C5b-7 complexes did not induce PGI2 formation.
    • Addition of complement component C8 to C5b-7 complexes (forming C5b-8) caused a time- and dose-dependent PGI2 release without overt cell damage.
    • The complete terminal complement complex C5b-9 also enhanced PGI2 release but induced cytolysis.
    • Extracellular calcium was essential for C5b-8-dependent PGI2 formation, but physiological calcium channel blockers were ineffective.
    • Calmodulin inhibitors (W7, trifluoperazine) reduced C5b-8-dependent PGI2 generation, without affecting Ca2+ flux.
    • C5b-8 complexes significantly enhanced the passive influx of 45Ca2+ and other small molecules into endothelial cells.

    Conclusions:

    • Complement C5b-8 complexes can act as calcium bypass gates in endothelial cells.
    • The ensuing influx of calcium activates the arachidonic acid pathway, leading to PGI2 production.
    • This mechanism highlights a novel pathway for complement-mediated regulation of vascular tone and function, independent of cell lysis.