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人红细胞中富含补体受体1的囊泡的释放。

Release of vesicles enriched in complement receptor 1 from human erythrocytes.

作者信息

Pascual M, Lutz H U, Steiger G, Stammler P, Schifferli J A

机构信息

Laboratory of Immunonephrology, Centre Médical Universitaire, Geneva, Switzerland.

出版信息

J Immunol. 1993 Jul 1;151(1):397-404.

PMID:8326133
Abstract

Vesicles released from human E by Ca(2+)-loading, ATP-depletion, or storage are enriched in several glycosylphosphatidylinositol-anchored proteins such as acetylcholinesterase (AchE) and decay-accelerating factor (DAF). As a result of this, the remaining E are depleted of these proteins. We analyzed whether vesiculation induced by ATP-depletion in vitro was also responsible for a loss of C receptor 1 (CR1), which is a transmembrane protein arranged predominantly in small clusters. ATP-depleted E had lost 15.4% to 33.9% of their CR1. This loss was similar to that of AchE and DAF. The released vesicles contained CR1. The number of CR1 per band 3 protein was 1.7 to 2.7 that in the original E, indicating an enrichment of CR1 in vesicles. This enrichment was similar to that observed for AchE and DAF (1.83- and 2.6-fold, respectively). The capacity of the vesicles and the ATP-depleted E to bind C3b-coated immune complexes correlated with the CR1 number, suggesting that there was no preferential loss of CR1 clusters. Vesicles released from human E during C attack also contained CR1. In conclusion, in vitro aging induced by ATP-depletion is responsible not only for a loss of glycosylphosphatidylinositol-anchored proteins, but also of CR1. Whether vesiculation explains the loss of CR1 from aging E in vivo and from E of patients with SLE or AIDS remains to be studied.

摘要

通过钙离子负载、ATP 耗竭或储存从人红细胞(E)释放的囊泡富含几种糖基磷脂酰肌醇锚定蛋白,如乙酰胆碱酯酶(AchE)和衰变加速因子(DAF)。由此导致的结果是,剩余的红细胞耗尽了这些蛋白。我们分析了体外 ATP 耗竭诱导的囊泡形成是否也导致 C 受体 1(CR1)的丢失,CR1 是一种主要以小簇形式排列的跨膜蛋白。ATP 耗竭的红细胞丢失了其 CR1 的 15.4%至 33.9%。这种丢失与 AchE 和 DAF 的丢失相似。释放的囊泡含有 CR1。每条带 3 蛋白上的 CR1 数量是原始红细胞中的 1.7 至 2.7 倍,表明 CR1 在囊泡中富集。这种富集与 AchE 和 DAF 观察到的富集相似(分别为 1.83 倍和 2.6 倍)。囊泡和 ATP 耗竭的红细胞结合 C3b 包被的免疫复合物的能力与 CR1 数量相关,表明不存在 CR1 簇的优先丢失。在补体攻击期间从人红细胞释放的囊泡也含有 CR1。总之,ATP 耗竭诱导的体外老化不仅导致糖基磷脂酰肌醇锚定蛋白的丢失,也导致 CR1 的丢失。囊泡形成是否解释了体内老化红细胞以及系统性红斑狼疮或艾滋病患者红细胞中 CR1 的丢失仍有待研究。

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