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Terminal complement complex and endothelial cells.

N Suttorp¹, S Bhakdi

¹Department of Internal Medicine, University of Giessen, FRG.

Zeitschrift Fur Kardiologie

|January 1, 1989

Summary

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The terminal complement sequence C5b-8 activates endothelial cells, increasing permeability and prostacyclin (PGI2) release via calcium influx, independent of known calcium channels. This suggests a novel C5b-8 mediated calcium-bypass mechanism.

Area of Science:

Immunology
Cell Biology
Physiology

Background:

The terminal complement sequence plays a role in immune responses and inflammation.
Endothelial cell functions, including prostacyclin (PGI2) generation and monolayer permeability, are critical for vascular health.

Purpose of the Study:

To investigate the effects of the terminal complement sequence on endothelial cell prostacyclin (PGI2) generation and monolayer permeability.
To elucidate the role of calcium influx in complement-mediated endothelial cell activation.

Main Methods:

Antibody-sensitized pulmonary artery endothelial cells were utilized.
Exposure to complement complexes (C5b-7, C5b-8, C5b-9) and measurement of PGI2 generation and endothelial permeability.
Assessment of extracellular calcium requirement and the effect of calcium channel blockers.

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Measurement of 45Ca2+ and other solute influx using radiolabeled tracers.

Main Results:

C5b-7 induced PGI2 formation without increasing permeability.
C5b-8 significantly increased PGI2 release and endothelial permeability, requiring extracellular Ca2+.
C5b-9 enhanced PGI2 release but caused cytolysis.
C5b-8 mediated a rapid, enhanced influx of Ca2+ and small solutes, bypassing physiological calcium channels.
Calcium channel blockers did not inhibit C5b-8 induced effects.

Conclusions:

Complement C5b-8 complexes act as calcium-bypass gates in endothelial cells.
The ensuing calcium influx activates the arachidonic acid pathway and actin-myosin system, leading to increased permeability.
This mechanism contributes to complement-mediated endothelial dysfunction.