CD59型
内化
补体系统
炎症
阻塞性睡眠呼吸暂停
缺氧(环境)
医学
间歇性缺氧
补体膜攻击复合物
免疫学
内科学
受体
化学
抗体
有机化学
氧气
作者
Memet Emin,Gang Wang,F. Castagna,Josanna Rodriguez-Lopez,Romina Wahab,Jing Wang,Tessa Adams,Ying Wei,Sanja Jelić
出处
期刊:Science Translational Medicine
[American Association for the Advancement of Science (AAAS)]
日期:2016-01-06
卷期号:8 (320)
被引量:38
标识
DOI:10.1126/scitranslmed.aad0634
摘要
Obstructive sleep apnea (OSA), characterized by intermittent hypoxia (IH) during transient cessation of breathing, triples the risk for cardiovascular diseases. We used a phage display peptide library as an unbiased approach to investigate whether IH, which is specific to OSA, activates endothelial cells (ECs) in a distinctive manner. The target of a differentially bound peptide on ECs collected from OSA patients was identified as CD59, a major complement inhibitor that protects ECs from the membrane attack complex (MAC). A decreased proportion of CD59 is located on the EC surface in OSA patients compared with controls, suggesting reduced protection against complement attack. In vitro, IH promoted endothelial inflammation predominantly via augmented internalization of CD59 and consequent MAC deposition. Increased internalization of endothelial CD59 in IH appeared to be cholesterol-dependent and was reversed by statins in a CD59-dependent manner. These studies suggest that reduced complement inhibition may mediate endothelial inflammation and increase vascular risk in OSA patients.
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