Yamaguchi Y, Matsumura F, Takeya M, Ichiguchi O, Kuratsu J I, Horiuchi T, Akizuki E, Matsuda T, Okabe K, Ohshiro H, Liang J, Mori K, Yamada S, Takahashi K, Ogawa M
Department of Surgery II, Kumamoto University Medical School, Japan.
Hepatology. 1998 Mar;27(3):727-34. doi: 10.1002/hep.510270314.
Intercellular adhesion molecule-1 (ICAM-1) is important in neutrophil-dependent injury. We investigated the effects of monocyte chemoattractant protein-1 (MCP-1) produced by Kupffer cells on ICAM-1 expression after ischemia-reperfusion in rat liver by occluding the portal vein for 30 minutes. Serum concentrations of MCP-1 increased persistently. By Northern analysis, MCP-1 mRNA increased early and persisted. Kupffer cells harvested 6 hours after reperfusion also expressed this transcript. The transcript and protein also were produced by Kupffer cells from naive controls in response to reactive oxygen species. ICAM-1 mRNA transcripts increased, peaked 3 hours after reperfusion, and decreased gradually thereafter. The level of ICAM-1 mRNA transcripts in the WK-5 rat endothelial cell line were markedly enhanced by MCP-1. These results suggest that MCP-1 released by Kupffer cells early after ischemia-reperfusion modulates neutrophil-dependent tissue injury via ICAM-1.
细胞间黏附分子-1（ICAM-1）在中性粒细胞依赖性损伤中起重要作用。我们通过阻断大鼠门静脉30分钟，研究了库普弗细胞产生的单核细胞趋化蛋白-1（MCP-1）对肝脏缺血再灌注后ICAM-1表达的影响。血清MCP-1浓度持续升高。通过Northern分析，MCP-1 mRNA早期增加并持续存在。再灌注6小时后收获的库普弗细胞也表达该转录本。来自未处理对照的库普弗细胞在受到活性氧刺激后也产生该转录本和蛋白质。ICAM-1 mRNA转录本增加，在再灌注3小时后达到峰值，此后逐渐下降。MCP-1显著增强了WK-5大鼠内皮细胞系中ICAM-1 mRNA转录本的水平。这些结果表明，缺血再灌注后早期库普弗细胞释放的MCP-1通过ICAM-1调节中性粒细胞依赖性组织损伤。
