Statin-Induced Expression of Decay-Accelerating Factor Protects Vascular Endothelium Against Complement-Mediated Injury
نویسندگان
چکیده
منابع مشابه
Statin-induced expression of decay-accelerating factor protects vascular endothelium against complement-mediated injury.
Complement-mediated vascular injury is important in the pathophysiology of atherosclerosis and myocardial infarction. Because recent evidence shows that statins have beneficial effects on endothelial cell (EC) function independent of lipid lowering, we explored the hypothesis that statins modulate vascular EC resistance to complement through the upregulation of complement-inhibitory proteins. H...
متن کاملStatin-Induced Expression of Decay-Accelerating Factor Protects Vascular Endothelium
Complement-mediated vascular injury is important in the pathophysiology of atherosclerosis and myocardial infarction. Because recent evidence shows that statins have beneficial effects on endothelial cell (EC) function independent of lipid lowering, we explored the hypothesis that statins modulate vascular EC resistance to complement through the upregulation of complement-inhibitory proteins. H...
متن کاملInduction of decay-accelerating factor by cytokines or the membrane-attack complex protects vascular endothelial cells against complement deposition.
Vascular endothelium is continuously exposed to complement-mediated challenge, and this is enhanced during inflammation. Although the complement-regulatory proteins decay-accelerating factor (DAF), CD59, and membrane cofactor protein (MCP) protect endothelial cells (ECs) against complement-mediated injury, the control of their expression and relative contributions to vascular protection is uncl...
متن کاملThe intrinsic complement regulator decay-accelerating factor modulates the biological response to vascular injury.
OBJECTIVE To investigate whether the presence of decay-accelerating factor (or CD55), an intrinsic complement regulator, protects against the development of vascular disease, given that complement activation can affect leukocytes and platelets. METHODS AND RESULTS Leukocyte-platelet complexes are critical for the initiation and progression of atherosclerosis and restenosis; however, the mecha...
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Catabolism of free heme by heme oxygenase-1 (HO-1) generates carbon monoxide, biliverdin, and free iron (Fe). These end-products are responsible for much of the biologic activity of HO-1, including anti-inflammatory, antiapoptotic, antiproliferative, and antioxidant effects. We have identified an additional cytoprotective action, the regulation of complement activation, mediated via induction o...
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ژورنال
عنوان ژورنال: Circulation Research
سال: 2002
ISSN: 0009-7330,1524-4571
DOI: 10.1161/01.res.0000038151.57577.19