Transient changes in erythrocyte membrane permeability are induced by sublytic amounts of the complement membrane attack complex (C5b-9).
Transient changes in erythrocyte membrane permeability are induced by sublytic amounts of the complement membrane attack complex (C5b-9).
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DOI：
10.1182/blood.v81.1.200.bloodjournal811200
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发表时间：
1993
期刊：
影响因子：
20.3
通讯作者：
J. Halperin;A. Taratuska;M. Rynkiewicz;A. Nicholson‐Weller
中科院分区：
文献类型：
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作者：
J. Halperin;A. Taratuska;M. Rynkiewicz;A. Nicholson‐Weller
我们以前已经表明，亚溶解异源补体诱导红细胞膜通透性的大，但短暂的增加。我们现在报道，当红细胞是酵母聚糖激活的自体血清中的旁观者时，它们的Na+渗透性增加10倍，表明自体补体也可以诱导短暂的膜损伤。当我们通过使用由纯化组分组装的人C5 b-9分离补体的C5 b-9膜攻击复合物的作用时，我们发现存在最小的溶解但有效的Na+摄取。亚溶损伤红细胞在K+培养基中的悬浮液导致细胞溶解，这与细胞募集补偿性K+流出一致，这与人红细胞暴露于异源补体时观察到的情况相似。当细胞外Ca 2+受限时，以及当细胞暴露于Charybdotoxin（一种Ca（2+）激活的K+通道抑制剂）时，亚溶解性C5 b-9暴露也变得溶解。这表明C5 b-9病变的功能性终止需要Ca 2+。我们还发现，由Ca（2+）依赖性K+流出激活引起的膜超极化并不影响C5 b-9损伤的终止。因此，通过补体损伤的Ca 2+内流启动至少两种明显独立的适应性反应：（1）终止渗漏的过程;和（2）具有容量调节功能的K+流出。我们的数据支持潜在的亚溶C5 b-9病变作为自体红细胞的生理介质。
We have previously shown that sublytic heterologous complement induces large but transient increases in erythrocyte membrane permeability. We now report that when erythrocytes are bystanders in zymosan-activated autologous serum, they increase their Na+ permeability 10-fold, indicating that autologous complement can also induce transient membrane lesions. When we isolated the effect of the C5b-9 membrane attack complex of complement by using human C5b-9 assembled from purified components, we found there was minimal lysis but efficient Na+ uptake. Suspension of the sublytically damaged erythrocytes in K+ medium caused the cells to lyse, which is consistent with the cells recruiting a compensatory K+ efflux similar to that observed when human erythrocytes were exposed to heterologous complement. Sublytic C5b-9 exposure also became lytic when extracellular Ca2+ was limited and when the cells were exposed to charybdotoxin, an inhibitor of the Ca(2+)-activated K+ channel. This indicates that Ca2+ is required for the functional termination of the C5b-9 lesion. We also show that the membrane hyperpolarization resulting from activation of the Ca(2+)-dependent K+ efflux does not influence the termination of the C5b-9 lesion. Thus, the influx of Ca2+ through the complement lesion initiates at least two apparently independent adaptive responses: (1) a process that terminates the leak; and (2) a K+ efflux that has a volume regulatory function. Our data support the potential of the sublytic C5b-9 lesion to act as a physiologic mediator for autologous erythrocytes.