Hydrogen peroxide-induced increase in endothelial adhesiveness is dependent on ICAM-1 activation.
Hydrogen peroxide-induced increase in endothelial adhesiveness is dependent on ICAM-1 activation.
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过氧化氢诱导的内皮粘附性增加依赖于 ICAM-1 激活。
DOI：
10.1152/ajplung.1993.264.4.l406
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Malik,AB
中科院分区：
文献类型：
--
作者：
Lo,SK;Janakidevi,K;Lai,L;Malik,AB
吞噬细胞产生的活性氧自由基（ROS）促进人中性粒细胞（PMN）与人脐静脉内皮细胞（EC）的粘附。我们通过测定稳态细胞内粘附分子1（ICAM-1）mRNA和ICAM-1蛋白表达来确定过氧化氢（H2 O2）（一种吞噬细胞来源的ROS）对EC粘附的影响。PMN对H2 O2处理的EC的粘附是浓度依赖性的，在0.1 mM H2 O2时达到最大粘附。PMN粘附迅速发生，在1小时的治疗时间内达到最大值。PMN粘附依赖于PMN表面的CD 11/CD 18整合素和EC表面的ICAM-1之间的相互作用，因为抗CD 18或抗ICAM-1单克隆抗体（MAbs）抑制PMN与EC之间的粘附作用（> 90%）。与EC粘附性的增加平行，我们检测到H2 O2攻击后0.5和1小时之间EC表面ICAM-1表达增加了2 - 3倍。北方分析显示，H2 O2暴露后0.5小时内，稳态ICAM-1 mRNA信号增加，并且该反应持续至2小时。3-amino-1，2，3-triazole抑制H2 O2处理的EC中的细胞内过氧化氢酶可使PMN粘附增加20%，而通过加入过氧化氢酶增强EC H2 O2清除活性可消除H2 O2诱导的PMN粘附，表明EC界面的氧化-抗氧化平衡是调节PMN-EC粘附相互作用的关键因素。结果提示，H_2O_2诱导的PMN粘附依赖于ICAM-1 mRNA信号的快速诱导和ICAM-1在EC表面的表达。（250字处删节）
Reactive oxygen radicals (ROS) generated by phagocytes promote human polymorphonuclear leukocyte (PMN) adhesion to human umbilical vein endothelial cells (EC). We determined the effects of hydrogen peroxide (H2O2), a phagocyte-derived ROS, on EC adhesiveness by determining steady-state intracellular adhesion molecule 1 (ICAM-1) mRNA and ICAM-1 protein expression. The adhesion of PMN to H2O2-treated EC was concentration dependent with maximal adhesion achieved at 0.1 mM H2O2. PMN adhesion occurred rapidly, reaching its maximum value within a 1-h treatment time. The PMN adhesion was dependent on the interaction between CD11/CD18 integrins on PMN and ICAM-1 on EC, since either anti-CD18 or anti-ICAM-1 monoclonal antibodies (MAbs) inhibited (by > 90%) the adhesive interaction between PMN and EC. In parallel with the increases in EC adhesivity, we detected a two- to threefold increase in EC surface expression of ICAM-1 between 0.5 and 1 h after H2O2 challenge. Northern analysis revealed an increase in the steady-state ICAM-1 mRNA signal within 0.5 h after H2O2 exposure, and the response was sustained up to 2 h. Inhibition of intracellular catalase in H2O2-treated EC by 3-amino-1,2,3-triazole augmented the PMN adhesion by 20%, whereas enhancement of EC H2O2-scavenging activity by addition of catalase abrogated the H2O2-induced PMN adhesion, indicating that oxidant-antioxidant balance at the EC interface is a critical factor modulating PMN-EC adhesive interactions. The results suggest that H2O2-induced PMN adhesion is dependent on the rapid induction of the ICAM-1 mRNA signal and the surface expression of ICAM-1 on EC.(ABSTRACT TRUNCATED AT 250 WORDS)