Bucki R, Bachelot-Loza C, Zachowski A, Giraud F, Sulpice J C
Laboratoire des Biomembranes et Messagers Cellulaires, CNRS ERS 571, Université Paris, France.
Biochemistry. 1998 Nov 3;37(44):15383-91. doi: 10.1021/bi9805238.
The increase in intracellular Ca2+ concentration in erythrocytes and platelets results in simultaneous phospholipid scrambling and microvesicle shedding. Microvesicle formation involves membrane fusion events which were proposed either to be tightly linked to phospholipid transversal redistribution or to occur by a separate mechanism. We report here that in erythrocytes incubated in high K+ medium, or in resealed ghosts, phospholipid scrambling can be fully induced by intracellular Ca2+ without microvesicle formation. Furthermore, in ghosts resealed in the presence of spermine, intracellular Ca2+, at low concentration, was able to induce microvesicles, whereas scrambling was drastically inhibited. Surprisingly, in spermine-containing ghosts prepared from erythrocytes of a patient with a bleeding disorder, due to a lack of Ca2+-induced phospholipid scrambling and vesicle shedding (characterized as a Scott syndrome), Ca2+ also promoted microvesicle release. Data show that phospholipid scrambling and microvesicle production, although closely regulated, proceed by independent pathways.
红细胞和血小板细胞内钙离子浓度的升高会导致磷脂同时发生翻转和微泡脱落。微泡形成涉及膜融合事件，这些事件要么被认为与磷脂横向重新分布紧密相关，要么通过单独的机制发生。我们在此报告，在高钾培养基中孵育的红细胞或重封的血影中，细胞内钙离子可完全诱导磷脂翻转而不形成微泡。此外，在存在精胺的情况下重封的血影中，低浓度的细胞内钙离子能够诱导微泡形成，而翻转则受到显著抑制。令人惊讶的是，在一名出血性疾病患者的红细胞制备的含精胺血影中，由于缺乏钙离子诱导的磷脂翻转和囊泡脱落（特征为斯科特综合征），钙离子也促进了微泡释放。数据表明，磷脂翻转和微泡产生虽然受到密切调控，但通过独立的途径进行。
