
<ArticleTitle>Complement components, but not complement inhibitors, are upregulated in atherosclerotic plaques.</ArticleTitle>
<AbstractText>Complement activation occurs in atherosclerotic plaques. The capacity of arterial tissue to inhibit this activation through generation of the complement regulators <prot>C1 inhibitor</prot>, <prot>decay accelerating factor</prot>, membrane cofactor protein (<prot>CD46</prot>), <prot>C4 binding protein</prot> (<prot>C4BP</prot>), and <prot>protectin</prot> (<prot>CD59</prot>) was evaluated in pairs of aortic atherosclerotic plaques and nearby normal artery from 11 human postmortem specimens. All 22 samples produced mRNAs for each of these proteins. The ratios of plaque versus normal artery pairs was not significantly different from unity for any of these inhibitors. However, in plaques, the mRNAs for <prot>C1r</prot> and <prot>C1s</prot>, the substrates for the <prot>C1 inhibitor</prot>, were increased 2.35- and 4.96-fold, respectively, compared with normal artery; mRNA for <prot>C4</prot>, the target for <prot>C4BP</prot>, was elevated l.34-fold; and mRNAs for <prot>C7</prot> and <prot>C8</prot>, the targets for <prot>CD59</prot>, were elevated 2.61- and 3.25-fold, respectively. By Western blotting and immunohistochemistry, fraction Bb of <prot>factor B</prot>, a marker of alternative pathway activation, was barely detectable in plaque and normal arterial tissue. These data indicate that it is primarily the classical, not the alternative pathway, that is activated in plaques and that key inhibitors are not upregulated to defend against this activation.</AbstractText>
