Apolipoprotein C-III in the high-density lipoprotein proteome of cerebral lacunar infarction patients impairs its anti-inflammatory function
Apolipoprotein C-III in the high-density lipoprotein proteome of cerebral lacunar infarction patients impairs its anti-inflammatory function
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DOI：
10.3892/ijmm.2017.3216
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发表时间：
2018-01-01
影响因子：
5.4
通讯作者：
Huang, Yining
中科院分区：
文献类型：
--
作者：
Lv, Pu;Zhao, Mingming;Huang, Yining
高密度脂蛋白（HDL）蛋白质组学研究已经确定了与各种疾病状态相关的实质性变化。本研究对腔隙性脑梗死（LACI）患者和对照组的HDL蛋白质组进行了研究。共有12例LACI患者（无明显大血管闭塞）和12例对照入组研究。通过超离心从血浆中分离来自每个样品的HDL部分。使用纳米液相色谱-串联质谱法研究HDL的蛋白质组学。在LACI组和对照组中有55种蛋白质被鉴定为差异表达。在55种蛋白质中，33种在LACI患者中表达上调，22种表达下调。所鉴定的蛋白质与许多分子功能相关，包括脂质和胆固醇转运、脂质代谢、炎症反应、补体和凝血途径、金属离子代谢、止血和内肽酶抑制活性。选择血清淀粉样蛋白A、载脂蛋白C（apoC-III）和载脂蛋白A-II（apoA-II）通过蛋白质印迹法证实蛋白质组学结果。与对照组相比，LACI患者HDL抑制THP-1细胞与内皮细胞结合的能力受损（P
High-density lipoprotein (HDL) proteomic study has identified substantial changes associated with various disease states. In the current study, the HDL proteomes in patients with cerebral lacunar infarction (LACI) and control subjects were investigated. A total of 12 LACI patients without evident large vessel occlusions and 12 controls were enrolled in the study. The HDL fraction from each sample was isolated from the plasma by ultracentrifugation. The protemics of the HDL were investigated using nano liquid chromatography coupled to tandem mass spectrometry. There were 55 proteins identified as differentially expressed in the LACI and control groups. Among the 55 proteins, 33 were upregulated and 22 were downregulated in the patients with LACI. The identified proteins were associated with numerous molecular functions, including lipid and cholesterol transport, lipid metabolism, inflammatory response, the complement and coagulation pathway, metal ion metabolism, hemostasis and endopeptidase inhibitory activity. Serum amyloid A, apolipoprotein C (apoC-III) and apolipoprotein A-II (apoA-II) were selected to confirm the proteomics results via western blotting. HDL from the LACI patients exhibited an impaired ability to inhibit the binding of THP-1 cells to endothelial cells compared with the controls (P