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PubMed · 2515670

Terminal complement complex and endothelial cells.

N Suttorp·S Bhakdi
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Abstract

The effects of the terminal complement sequence on two endothelial cell functions (prostacyclin (PGI2) generation and permeability of an endothelial cell monolayer) were examined in antibody-sensitized pulmonary artery endothelial cells. Whereas C5b-7 complement complexes induced on PGI2 formation and no enhanced endothelial permeability, addition of purified complement component C8 resulted in a time- and dose-dependent burst of PGI2 release and in a substantially increased permeability of an endothelial cell monolayer in the absence of overt cell damage. Formation of the complete terminal complement complex C5b-9 enhanced PGI2 release but was accompanied by cytolysis. Extracellular Ca2+ was required for C5b-8 dependent PGI2 formation. Three different blockers of physiological calcium channels failed to suppress the observed stimulatory effect. One minute after addition of C8 to endothelial cells carrying C5b-7 complexes, a six to sevenfold enhanced passive influx of 45Ca2+ into the cells was noted. An enhanced passive influx was also observed for 51CrO4(2-), 3H-aminobutyric acid, and 3H-sucrose, but not for 3H-inulin and 3H-dextran. These data together suggest that complement C5b-8 complexes may serve as Ca2+-bypass gates in endothelial cells, the ensuing influx of Ca2+ leading to subsequent activation of the arachidonic acid pathway and the actin-myosin system.

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Arachidonic AcidArachidonic AcidsCell Membrane PermeabilityCells, CulturedComplement ActivationComplement C5Complement C5bEndothelium, VascularEpoprostenolHumansJournal Article

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N Suttorp, S Bhakdi. 1989. Terminal complement complex and endothelial cells.. https://pubmed.ncbi.nlm.nih.gov/2515670/

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