Ferrell J E, Huestis W H
J Cell Biol. 1984 Jun;98(6):1992-8. doi: 10.1083/jcb.98.6.1992.
ATP-depleted human erythrocytes lose their smooth discoid shape and adopt a spiny, crenated form. This shape change coincides with the conversion of phosphatidylinositol-4,5-bisphosphate to phosphatidylinositol and phosphatidic acid to diacylglycerol. Both crenation and lipid dephosphorylation are accelerated by iodoacetamide, and both are reversed by nutrient supplementation. The observed changes in lipid populations should shrink the membrane inner monolayer by 0.6%, consistent with estimates of bilayer imbalance in crenated cells. These observations suggest that metabolic crenation arises from a loss of inner monolayer area secondary to the degradation of phosphatidylinositol-4,5-bisphosphate and phosphatidic acid. A related process, crenation after Ca2+ loading, appears to arise from a loss inositides by a different pathway.
ATP 耗尽的人类红细胞会失去其光滑的盘状形态,转而呈现出多刺的锯齿状形态。这种形态变化与磷脂酰肌醇 -4,5- 二磷酸转化为磷脂酰肌醇以及磷脂酸转化为二酰基甘油同时发生。碘乙酰胺会加速锯齿状形成和脂质去磷酸化,而营养补充则可使其逆转。观察到的脂质群体变化应会使膜内单层收缩 0.6%,这与锯齿状细胞中双层膜失衡的估计相符。这些观察结果表明,代谢性锯齿状形成源于磷脂酰肌醇 -4,5- 二磷酸和磷脂酸降解导致的内单层面积损失。一个相关过程,即 Ca2+ 加载后的锯齿状形成,似乎是通过不同途径导致肌醇磷脂损失而产生的。