中文摘要：

这研究的目的是构造包含特别地绑与的 scavenger 受体(SR-PSOX ) 的 lentiviral 表达式向量有六个 histidine 标签并且到的 phosphatidylserine 和氧化脂蛋白在动脉粥样硬化调查 SR-PSOX 的函数。我们利用有效在 vitro 或 invivo 交付目标基因进用提高的 biosafetyreplication 无能的 lentivirus 划分和非划分的哺乳动物的房间的 ViraPower lentiviral 表达式系统。钝结束的顺序用克隆反应的 reversetranscription 聚合酶链反应和方向性的 TOPO 被放大。通过一双 thecytomegalovirus 提交教材和 SR-PSOX 的反向的教材，正确克隆被聚合酶链反应识别并且定序。包装混合 andSR-PSOX-pLenti6/V5 TOPO 表示原生质标志的 ViraPower 是进 293FT 房间线 usingLipofectamine 的 co-transfected 2000。内长、外长的 SR-PSOX 以及在在不同时间的各种各样的泡沫房间模型的 - α蛋白质削尖的肿瘤坏死因素(TNF ) 的表示被 sodiumdodecyl sulfate-polyacrylamide 凝胶电泳，蛋白质印迹和间接 immunofluorescenceassay 检测。蛋白质印迹和免疫荧光分析证实α蛋白质是起来的 SR-PSOX andTNF- 的表情在泡沫房间模型调整了。我们的数据建议过去表示 ofrecom-binant 人 SR-PSOX 蛋白质能支持泡沫房间形成并且起来调整煽动性的因素 TNF- α的表示。

英文摘要：

The aim of this study is to construct a lentiviral expression vector containing a scavenger receptor （SR-PSOX） that binds with uniquely phosphatidylserine and oxidized lipoprotein with six histidine tags and to investigate the function of SR-PSOX in atherosclerosis. We utilize the ViraPower lentiviral expression system which was efficient to deliver in vitro or in vivo the target gene into dividing and nondividing mammalian cells using an enhanced biosafety replication-incompetent lentivirus. The blunt-end sequence was amplified using the reverse transcription-polymerase chain reaction and directional TOPO cloning reaction. Through a pair of the cytomegalovirus forward primer and the reverse primer of SRPSOX, the correct clones were identified by polymerase chain reaction and sequencing. The ViraPower packaging mix and SR-PSOX-pLenti6/V5 TOPO expression plasmid were co-transfected into the 293FT cell line using Lipofectamine 2000. The expression of endogenous and exogenous SR-PSOX as well as tumor necrosis factor （TNF）-α protein in various foam cell models at different time points were detected by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, Western blot and indirect immunofluorescence assay. Western blot and immunofluorescence analysis confirmed that the expressions of SR-PSOX and TNF-o~ protein were upregulated in foam cell models. Our data suggested that the overexpression of recombinant human SR-PSOX protein can promote foam cell formation and upregulate the expression of the inflammatory factor TNF-α.