Abstract:
BACKGROUND:Interaction of complement with endothelial cells (ECs) underlies the development of inflammation and coagulation in disease. Assembly of the membrane attack complex (MAC) of complement on EC membrane, like stimulation with cytokines, upregulates tissue factor and cyclooxygenase-2 but does so via the intermediary action of IL-1alpha. We asked whether the MAC activates porcine aortic and microvascular ECs in a global manner by this mechanism and whether this mechanism is used by membrane pore-forming structures. METHODS AND RESULTS:Exposure of ECs to complement caused upregulation of mRNAs for E-selectin, intracellular adhesion molecule-1, vascular cell adhesion molecule-1, Ikappa-Balpha, interleukin (IL)-1alpha, IL-1beta, IL-8, and plasminogen activator inhibitor-1 over a period of 6 hours. The expression of these genes was not a primary response to stimulation, however, because IL-1 receptor antagonist inhibited expression of these genes. Activation of ECs by complement depended on the autocrine action of IL-1alpha, because complement-mediated EC activation was inhibited by anti-IL-1alpha antibodies. Melittin and mastoparan, amphiphilic pore-forming peptides like the MAC, induced E-selectin through intermediary action of IL-1. CONCLUSIONS:These findings suggest that transmembrane pore-forming proteins, as a class of molecules, activate ECs through the autocrine effects of IL-1alpha.
journal_name
Circulationjournal_title
Circulationauthors
Saadi S,Holzknecht RA,Patte CP,Platt JLdoi
10.1161/01.cir.101.15.1867subject
Has Abstractpub_date
2000-04-18 00:00:00pages
1867-73issue
15eissn
0009-7322issn
1524-4539journal_volume
101pub_type
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