Increased Plasma Levels of Microparticles Expressing CD39 and CD133 in Acute Liver Injury
Increased Plasma Levels of Microparticles Expressing CD39 and CD133 in Acute Liver Injury
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DOI：
10.1097/tp.0b013e318278d3cd
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发表时间：
2013-01-15
期刊：
影响因子：
6.2
通讯作者：
Robson, Simon C.
中科院分区：
文献类型：
--
作者：
Schmelzle, Moritz;Splith, Katrin;Robson, Simon C.
背景资料。我们先前已经证明，CD133和CD39是由造血干细胞(HSC)表达的，HSC在肝损伤和损伤靶点动员，限制血管炎症，促进肝再生。表达CD39的血浆微粒(MP)可阻断内皮细胞活化。在这里，我们测试了CD133(+)MP是否可能在肝损伤模型中以CD39依赖的方式脱落，并在临床上潜在地作为肝功能衰竭的生物标志物。野生型和CD39基因缺失的小鼠造成扑热息痛诱导的肝损伤。处死小鼠，超速离心法分离血浆MP。荧光激活细胞分选法分析HSC和CD133(+)MP水平。急性肝损伤患者(n=5)和慢性急性肝损伤患者(n=5)与对照组(n=7)。入院时采血，用荧光激活细胞分选法分析血浆CD133(+)和CD39(+)MP亚群。仅扑热息痛肝毒性野生型小鼠血浆HSC和CD133(+)MP水平显著升高(P
Background. We have previously demonstrated that CD133 and CD39 are expressed by hematopoietic stem cells (HSC), which are mobilized after liver injury and target sites of injury, limit vascular inflammation, and boost hepatic regeneration. Plasma microparticles (MP) expressing CD39 can block endothelial activation. Here, we tested whether CD133(+) MP might be shed in a CD39-dependent manner in a model of liver injury and could potentially serve as biomarkers of liver failure in the clinic.Methods. Wild-type and Cd39-null mice were subjected to acetaminophen-induced liver injury. Mice were sacrificed and plasma MP were isolated by ultracentrifugation. HSC and CD133(+) MP levels were analyzed by fluorescence-activated cell sorting. Patients were enrolled with acute (n=5) and acute on chronic (n=5) liver injury with matched controls (n=7). Blood was collected at admission and plasma CD133(+) and CD39(+) MP subsets were analyzed by fluorescence-activated cell sorting.Results. HSC and CD133(+) MP levels were significantly increased only in the plasma of wild-type mice with acetaminophen hepatotoxicity (P