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首页> 外文期刊>Journal of Cellular Physiology >Role of LOX-1 in monocyte adhesion-triggered redox, Akt/eNOS and Ca2+ signaling pathways in endothelial cells.
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Role of LOX-1 in monocyte adhesion-triggered redox, Akt/eNOS and Ca2+ signaling pathways in endothelial cells.

机译:在单核adhesion-triggered LOX-1的角色氧化还原,Akt /以挪士和Ca2 +的信号通路内皮细胞。

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This study was conducted to examine the role of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) in monocyte adhesion-induced redox-sensitive, Akt/eNOS and Ca2+ signaling pathways in endothelial cells (ECs). LOX-1 was blocked by an antibody-neutralizing LOX-1 TS92 or small interfering RNA. In cultured human aortic ECs, monocyte adhesion activated Rac1 and p47(phox), and increased NADPH oxidase activity and reactive oxygen species (ROS) generation within 30 min and NF-kappaB phosphorylation within 1 h, resulting in redox-sensitive gene expression. Akt and eNOS phosphorylation was induced 15 min after adding monocytes and returned to control level after 30 min, whereas NO production was not altered by monocyte adhesion. Blockade of LOX-1 blunted the monocyte adhesion-triggered redox-sensitive signaling pathway and Akt/eNOS phosphorylation in ECs. Both endothelial intracellular Ca2+ mobilization and Ca2+ influx caused by monocyte attachment were markedly attenuated by pretreatment of ECs with TS92. This suggests that LOX-1 is involved in redox-sensitive, Akt/eNOS and Ca2+ signaling pathways in monocyte adhesion to ECs independent of oxidized low-density lipoprotein (ox-LDL). Furthermore, blockade of Ca2+ inhibited monocyte adhesion-triggered Rac1 and p47(phox) activation and ROS generation in ECs, whereas Ca2+ signaling was suppressed by blockade of NADPH oxidase and ROS generation. Finally, TS92 blocked the monocyte adhesion to ECs stimulated with or without tumor necrosis factor-alpha or ox-LDL. We provide evidence that LOX-1 plays a role in redox-sensitive, Akt/eNOS and Ca2+ signaling pathways in monocyte adhesion to ECs independent of the ox-LDL-LOX-1 axis.
机译:本研究进行了检查的作用lectin-like氧化低密度脂蛋白在单核adhesion-induced receptor-1 (LOX-1)redox-sensitive, Akt /以挪士和Ca2 +信号在内皮细胞通路(ECs)。被一个antibody-neutralizing LOX-1 TS92或小干扰RNA。Rac1和ECs,单核细胞粘附激活p47 (phox),并增加NADPH氧化酶活性和活性氧(ROS)生成在30分钟内和NF-kappaB磷酸化在1 h,导致redox-sensitive基因表达式。诱导增加单核细胞和后15分钟30分钟后回到控制水平,而不生产不被单核细胞改变附着力。adhesion-triggered redox-sensitive信号ECs的途径和一种蛋白激酶/以挪士磷酸化。内皮细胞内钙离子动员和Ca2 +涌入造成的单核细胞附件预处理明显减毒的ECsTS92。redox-sensitive, Akt /以挪士和Ca2 +信号通路在单核细胞粘附ECs独立氧化的低密度脂蛋白(ox-LDL)。此外,Ca2 +抑制单核细胞的封锁adhesion-triggered Rac1和p47 (phox)激活ECs和活性氧生成,而钙离子信号被封锁NADPH氧化酶和镇压ROS生成。单核细胞粘附ECs与或刺激没有肿瘤坏死因子-α和ox-LDL。提供证据证明LOX-1起着作用redox-sensitive, Akt /以挪士和Ca2 +信号通路在单核细胞粘附ECs独立ox-LDL-LOX-1轴。

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