STABILIZING FACTORS OF PHOSPHOLIPID ASYMMETRY IN THE ERYTHROCYTE-MEMBRANE
STABILIZING FACTORS OF PHOSPHOLIPID ASYMMETRY IN THE ERYTHROCYTE-MEMBRANE
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DOI：
10.1016/0005-2736(84)90170-6
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发表时间：
1984-01-01
期刊：
影响因子：
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通讯作者：
ERUSALIMSKY, JD
中科院分区：
文献类型：
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作者：
DRESSLER, V;HAEST, CWM;ERUSALIMSKY, JD
研究了外源性溶血磷脂在人红细胞和膜泡中的跨双层重定向（翻转）和内源性磷脂跨双层分布的变化。(1)外源性溶血磷脂酰丝氨酸在人红细胞重封血影的内膜层中不可逆地蓄积。(2)这种积累甚至发生在完全丧失内源性磷脂酰乙醇胺的不对称分布和磷脂酰丝氨酸不对称性的部分损失后，在二酰胺处理的细胞。(3)从红细胞膜形成的内面向外和正面向外的囊泡导致内源性磷脂不对称性的丧失以及建立外源性溶血磷脂酰丝氨酸不对称性的能力的丧失。然而，溶血磷脂的囊泡的transbilayer重定向率，是那些完整的细胞。(4)在血影蛋白热变性后从红细胞分离的囊泡中也观察到磷脂酰丝氨酸内源性不对称性的丧失。残留细胞中的不对称性得以维持。(5)与磷脂酰乙醇胺和磷脂酰丝氨酸的不对称性的丧失相反，鞘磷脂的不对称性完全保持在囊泡中。(6)磷脂的不对称性在本机细胞中的稳定性进行了讨论，在一个假设的重定向位点的磷脂访问的限制。这种限制可能是磷脂与膜骨架相互作用的结果，如在磷脂酰丝氨酸和磷脂酰乙醇胺的情况下，或者是脂质-脂质相互作用的结果，如在鞘磷脂的情况下。
Transbilayer reorientation (flip) of exogenous lysophospholipids and changes of the transbilayer distribution of endogenous phospholipids were studied in human erythrocytes and membrane vesicles. (1) Exogenous lysophosphatidylserine irreversibly accumulates in the inner membrane layer of resealed ghosts of human erythrocytes. (2) This accumulation even occurs after complete loss of asymmetric distribution of endogenous phosphatidylethanolamine and partial loss of phosphatidylserine asymmetry in diamide-treated cells. (3) Formation of inside-out and right-side-out vesicles from erythrocyte membranes results in a loss of endogenous phospholipid asymmetry as well as of the ability to establish asymmetry of exogenous lysophosphatidylserine. Rates of transbilayer reorientation of lysophospholipids for the vesicles, however, are comparable to those for intact cells. (4) Loss of endogenous asymmetry of phosphatidylserine is also observed in vesicles isolated from erythrocytes after heat denaturation of spectrin. The asymmetry in the residual cells is maintained. (5) In contrast to the loss of asymmetry of phosphatidylethanolamine and of phosphatidylserine, the asymmetry of sphingomyelin is completely maintained in the vesicles. (6) The stability of phospholipid asymmetry in the native cell is discussed in terms of a limitation of access of phospholipids to hypothetical reorientation sites. Such a limitation may either be the result of interaction of phospholipids with the membrane skeleton as in case of phosphatidylserine and phosphatidylethanolamine, or the result of lipid-lipid interactions as in case of sphingomyelin.