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Related Experiment Videos

Consecutive enzyme cascades: complement activation at the cell surface triggers increased tissue factor activity.

S D Carson1, D R Johnson

  • 1Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha 68198-6495.

Blood
|July 15, 1990
PubMed
Summary
This summary is machine-generated.

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Antibody-mediated complement activation on cell surfaces triggers tissue factor activity and cell damage. This process directly stimulates the coagulation cascade, leading to fibrin clot formation following immunologically mediated cell injury.

Area of Science:

  • Immunology
  • Cell Biology
  • Hematology

Background:

  • Complement activation at the cell surface causes cell damage via membrane attack complex assembly and cytoplasmic leakage.
  • Cell membrane damage, whether chemical or physical, is known to rapidly increase tissue factor procoagulant activity.

Purpose of the Study:

  • To investigate the relationship between antibody-mediated complement activation on cell surfaces and the subsequent expression of tissue factor activity.
  • To determine if complement fixation directly impacts the coagulation cascade initiation.

Main Methods:

  • Antibody-mediated complement activation was induced on cell surfaces.
  • Tissue factor activity was measured.
  • Cytolysis was assessed using 51-chromium release assays.

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Main Results:

  • Complement activation at the cell surface led to increased tissue factor activity.
  • This increase in tissue factor activity correlated with the degree of cytolysis observed.
  • The study demonstrated a direct link between complement fixation and tissue factor upregulation.

Conclusions:

  • Complement fixation on cell surfaces can directly and immediately stimulate the coagulation cascade.
  • Immunologically mediated cell damage initiates a rapid procoagulant response.
  • Fibrin clot formation can occur rapidly following complement-mediated cell damage.