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Complement C5b-9 increases plasminogen binding and activation on human endothelial cells

V J Christiansen1, P J Sims, K K Hamilton

  • 1Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City 73190, USA. vicki.christiansen@cclink.net.UOKHSC.edu

Arteriosclerosis, Thrombosis, and Vascular Biology
|January 1, 1997
PubMed
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Complement C5b-9 deposition on endothelial cells enhances plasminogen (PG) binding and activation. Membrane C9 may bind PG and boost tissue-type plasminogen activator (TPA) activity, impacting vessel wall function.

Area of Science:

  • Immunology
  • Cell Biology
  • Biochemistry

Background:

  • Terminal complement proteins (C5b-9) can alter endothelial cell function, including procoagulant responses.
  • Endothelial cells regulate fibrinolysis, the breakdown of blood clots.
  • C9 shares structural similarities with proteins that bind and activate plasminogen (PG).

Purpose of the Study:

  • To investigate the effects of complement injury on plasminogen binding and activation on human endothelial cells.
  • To determine if C5b-9 deposition influences plasminogen's interaction with endothelial cells.
  • To elucidate the role of C9 in plasminogen activation.

Main Methods:

  • Complement activation on human endothelial cells using C5b67 and C5b-9 complexes.
  • Measurement of specific 125I-plasminogen binding to endothelial cells.

Related Experiment Videos

  • Assay of plasminogen activation by tissue-type plasminogen activator (TPA) in cell-free systems and on cells.

    • Main Results:

    • C5b-9 deposition increased plasminogen binding by approximately 100%.
    • Plasminogen specifically bound to C7 and C9 components of the membrane attack complex.
    • Bound plasminogen was readily activated by TPA, and C9 enhanced this activation in a cell-free system.

    Conclusions:

    • Membrane C9 may provide a binding site for plasminogen.
    • C9 enhances plasminogen activation by TPA, potentially through its carboxyl-terminal lysine.
    • Immune-mediated endothelial injury may increase both fibrin generation and fibrinolysis on the vessel wall.