Breittmayer J P, Pelassy C, Aussel C
INSERM U343, Hôpital de l'Archet, Nice, France.
J Lipid Mediat Cell Signal. 1996 Mar;13(2):151-61. doi: 10.1016/0929-7855(95)00059-3.
CD3 mAb induced calcium movements are unaffected by hyperpolarization of the membrane in Jurkat T cells treated with valinomycin. By contrast, the CD3 induced Ca2+ influx was impaired by depolarization of the membrane with either gramicidin or by equimolar substitution of KCl for NaCl in the medium. In depolarized cells, the synthesis of phosphatidylserine was strongly diminished as a result of impaired transport of the [3H]serine substrate. In depolarized cells, the CD3-induced release of Ca2+ from intracellular stores (endoplasmic reticulum) was unaffected. Emptying of the Ca2+ stores by CD3 was shown by the lack of effect of additional treatment of the cells with the Ca2+ ionophore, ionomycin. The empty status of the calcium stores was also confirmed by measurements of phosphatyidylserine synthesis through the Ca2+ -dependent base exchange enzyme system that was found to be significantly decreased despite the low amount synthesized in the presence of a defective [3H]serine transport in depolarized cells.
在用缬氨霉素处理的Jurkat T细胞中，CD3单克隆抗体诱导的钙运动不受膜超极化的影响。相比之下，用短杆菌肽使膜去极化或在培养基中用等摩尔的KCl替代NaCl，都会损害CD3诱导的Ca2+内流。在去极化细胞中，由于[3H]丝氨酸底物转运受损，磷脂酰丝氨酸的合成显著减少。在去极化细胞中，CD3诱导的Ca2+从细胞内储存库（内质网）的释放不受影响。用Ca2+离子载体离子霉素对细胞进行额外处理没有效果，这表明CD3使Ca2+储存库排空。通过Ca2+依赖的碱基交换酶系统测量磷脂酰丝氨酸的合成，也证实了钙储存库的排空状态，尽管在去极化细胞中存在有缺陷的[3H]丝氨酸转运时合成的量很少，但发现该系统仍显著降低。
