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多磷酸肌醇与哺乳动物红细胞的形态

Polyphosphoinositides and the shape of mammalian erythrocytes.

作者信息

Quist E, Powell P

出版信息

Lipids. 1985 Jul;20(7):433-8. doi: 10.1007/BF02534234.

Abstract

The relationship between polyphosphoinositide and phosphatidic acid (PA) metabolism and Mg-ATP dependent shape and viscosity changes in erythrocyte ghosts from four mammalian species was examined. Ghosts prepared from rabbit, dog, human and guinea pig erythrocytes were transformed from echinocytes to discocytes within 15 min in the presence of 1 mM Mg-ATP at 25 C. In all species these Mg-ATP shape transformations were associated with a 30-45% decrease in the specific viscosity of the ghost suspensions. Mg-ATP induced a second transformation of discocytic ghosts to cup shape forms without a further decrease in viscosity. A considerable species variation in the rates of Mg-ATP dependent viscosity and shape changes and incorporation of 32P into phosphatidylinositol-4' phosphate (PIP), phosphatidylinositol-4'5'bisphosphate (PIP2) and especially PA from Mg-[gamma 32P]-ATP in ghosts was found. However, the rates of Mg-ATP dependent synthesis of PIP and PIP2 and shape and viscosity changes in each species were of the same magnitude. Ca2+ or neomycin strongly inhibited PIP labeling and Mg-ATP shape and viscosity changes in ghosts of the different species. Ca2+ or neomycin usually increased or had little effect on 32P incorporation into PA and PIP2. The possibility that Mg-ATP-induced changes in erythrocyte membrane shape and deformability are dependent on increases in membrane PIP and PIP2 is discussed.

摘要

研究了四种哺乳动物红细胞膜空壳中多磷酸肌醇与磷脂酸(PA)代谢之间的关系,以及Mg-ATP依赖性的形态和粘度变化。在25℃下,存在1 mM Mg-ATP时,由兔、狗、人及豚鼠红细胞制备的膜空壳在15分钟内从棘状细胞转变为盘状细胞。在所有物种中,这些Mg-ATP诱导的形态转变均伴随着膜空壳悬浮液比粘度降低30 - 45%。Mg-ATP诱导盘状膜空壳第二次转变为杯状形态,且粘度没有进一步降低。发现不同物种的膜空壳中,Mg-ATP依赖性粘度和形态变化速率以及32P掺入磷脂酰肌醇-4'-磷酸(PIP)、磷脂酰肌醇-4',5'-双磷酸(PIP2)尤其是从Mg-[γ32P]-ATP掺入PA的速率存在相当大的物种差异。然而,每个物种中Mg-ATP依赖性PIP和PIP2合成速率以及形态和粘度变化幅度相同。Ca2+或新霉素强烈抑制不同物种膜空壳中的PIP标记以及Mg-ATP诱导 的形态和粘度变化。Ca2+或新霉素通常会增加或对32P掺入PA和PIP2影响很小。讨论了Mg-ATP诱导红细胞膜形态和变形性变化是否依赖于膜PIP和PIP2增加的可能性。

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