The remote ischemic preconditioning stimulus modifies inflammatory gene expression in humans
The remote ischemic preconditioning stimulus modifies inflammatory gene expression in humans
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DOI：
10.1152/physiolgenomics.00046.2004
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发表时间：
2004-09-16
影响因子：
4.6
通讯作者：
Redington, AN
中科院分区：
文献类型：
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作者：
Konstantinov, IE;Arab, S;Redington, AN
远端缺血预适应(IPC)可减轻远隔器官缺血再灌注(IR)所致的组织损伤。我们测试了远程IPC(RIPC)修改人类炎症基因转录的假设。利用微阵列方法，我们证明了一种简单的前臂短暂缺血模型可以抑制循环白细胞中促炎症基因的表达。参与细胞因子合成、白细胞趋化、黏附和迁移、胞吐、先天免疫信号通路和细胞凋亡的关键蛋白编码基因在15min内(早期IPC)均受到抑制，在24 h后更明显(第二窗口IPC)。流式细胞仪检测的白细胞CD11b表达的变化反映了这一模式，在24 h时显著降低(P=0.01)。这种作用可能参与了IPC对IR损伤的保护作用，并可能在其他炎症过程中具有更广泛的意义。这是对RIPC刺激后人类基因表达的第一次研究。RIPC刺激抑制人白细胞中的致炎基因转录。
Remote ischemic preconditioning (IPC) reduces tissue injury caused by ischemia-reperfusion (IR) in distant organs. We tested the hypothesis that remote IPC (rIPC) modifies inflammatory gene transcription in humans. Using a microarray method, we demonstrated that a simple model of brief forearm ischemia suppresses proinflammatory gene expression in circulating leukocytes. Genes encoding key proteins involved in cytokine synthesis, leukocyte chemotaxis, adhesion and migration, exocytosis, innate immunity signaling pathways, and apoptosis were all suppressed within 15 min (early phase IPC) and more so after 24 h ( second window IPC). Changes in leukocyte CD11b expression measured by flow cytometry mirrored this pattern, with there being a significant ( P = 0.01) reduction at 24 h. The results of this study show that the rIPC stimulus modifies leukocyte inflammatory gene expression. This effect may contribute to the protective effect of IPC against IR injury and may have broader implications in other inflammatory processes. This is the first study of human gene expression following rIPC stimulus. rIPC stimulus suppressed proinflammatory gene transcription in human leukocytes.