Differential regulation of endothelial cell activation by complement and interleukin 1alpha.

ABSTRACT: Activation of complement on endothelium triggers physiological changes that promote coagulation, thrombosis, and inflammation. Unlike agonists such as cytokines and endotoxin that induce these changes through transcription of many genes, complement, particularly the membrane attack complex, primarily induces release of IL-1alpha by the endothelial cells; the cytokine may then be removed by normal blood flow or may promote activation of the full range of endothelial cell responses in an autocrine or paracrine manner. We studied the intracellular signaling pathways used by complement to activate interleukin (IL)-1alpha transcription in cultured endothelial cells. The membrane attack complex and other pore-forming proteins stimulated calcineurin and activated selective transcription of the IL

SUBMITTER: Brunn GJ 

PROVIDER: S-EPMC1513160 | biostudies-literature | 2006 Mar

REPOSITORIES: biostudies-literature