Thioredoxin reductase 1 upregulates MCP-1 release in human endothelial cells.
Thioredoxin reductase 1 upregulates MCP-1 release in human endothelial cells.
复制标题
硫氧还蛋白还原酶 1 上调人内皮细胞中 MCP-1 的释放。
DOI：
10.1016/j.bbrc.2009.06.100
复制
发表时间：
2009
影响因子：
3.1
通讯作者：
Xun Shen
中科院分区：
文献类型：
--
作者：
Zhen;Xun Shen
为了了解硫氧还蛋白还原酶1（TrxR 1）是否在抗动脉粥样硬化的抗氧化防御机制中发挥作用，研究了TrxR 1对活化的人内皮样EAhy 926细胞中单核细胞趋化蛋白（MCP-1）表达/释放的影响。在过表达重组TrxR 1或敲低内源性TrxR 1的细胞中检测MCP-1的释放和表达、细胞内活性氧（ROS）的产生、核转位和NF-κB亚基p65的DNA结合活性。发现TrxR 1的过表达增强，而TrxR 1的敲低降低MCP-1的释放和表达。TrxR 1上调MCP-1与细胞内ROS生成增加、核转位增强和NF-κB DNA结合活性增强有关。利用NF-κB报告基因检测显示TrxR 1上调NF-κB的转录活性。本研究提示TrxR 1可增强内皮细胞ROS生成、NF-κB活性及随后的MCP-1表达，可能促进而非阻止血管内皮形成动脉粥样硬化斑块。
To know if thioredoxin reductase 1 (TrxR1) plays a role in antioxidant defense mechanisms against atherosclerosis, effect of TrxR1 on expression/release of monocyte chemoattractant protein (MCP-1) was investigated in activated human endothelial-like EAhy926 cells. The MCP-1 release and expression, cellular generation of reactive oxygen species (ROS), nuclear translocation and DNA-binding activity of NF-κB subunit p65 were assayed in cells either overexpressing recombinant TrxR1 or having their endogenous TrxR1 knocked down. It was found that overexpression of TrxR1 enhanced, while knockdown of TrxR1 reduced MCP-1 release and expression. Upregulation of MCP-1 by TrxR1 was associated with increasing generation of intracellular ROS generation, enhanced nuclear translocation and DNA-binding activity of NF-κB. Assay using NF-κB reporter revealed that TrxR1 upregulated transcriptional activity of NF-κB. This study suggests that TrxR1 enhances ROS generation, NF-κB activity and subsequent MCP-1 expression in endothelial cells, and may promote rather than prevent vascular endothelium from forming atherosclerotic plaque.
影响因子：
2.9
作者：
Hill, KE;McCollum, GW;Burk, RF
通讯作者：
Burk, RF
DOI：
10.1073/pnas.0501719102
发表时间：
2005-04-19
影响因子：
11.1
作者：
Zhao, HT;Joseph, J;Kalyanaraman, B
通讯作者：
Kalyanaraman, B
DOI：
10.1152/ajpheart.00716.2003
发表时间：
2004-03-01
影响因子：
4.8
作者：
Chen, XL;Zhang, Q;Medford, RM
通讯作者：
Medford, RM