The remote ischemic preconditioning stimulus modifies inflammatory gene expression in humans

被引:287
作者
Konstantinov, IE
Arab, S
Kharbanda, RK
Li, J
Cheung, MMH
Cherepanov, V
Downey, GP
Liu, PP
Cukerman, E
Coles, JG
Redington, AN
机构
[1] Hosp Sick Children, Div Cardiol, Toronto, ON M5G 1X8, Canada
[2] Hosp Sick Children, Div Cardiovasc Surg, Toronto, ON M5G 1X8, Canada
[3] Univ Toronto, Toronto Gen Hosp, Div Cardiol Heart & Stroke, Richard Lewar Ctr Excellence, Toronto, ON M5G 1L7, Canada
[4] Univ Toronto, Toronto Gen Hosp, Div Respirol, Toronto, ON M5G 1L7, Canada
[5] Univ Cambridge, Addenbrookes Ctr Clin Invest, Cambridge, England
关键词
genes; inflammation; ischemia; leukocytes; reperfusion;
D O I
10.1152/physiolgenomics.00046.2004
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:143 / 150
页数:8
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