Porous red cell ultrastructure and loss of membrane asymmetry in a novel case of hemolytic anemia
Porous red cell ultrastructure and loss of membrane asymmetry in a novel case of hemolytic anemia
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DOI：
10.1111/j.1600-0609.2008.01153.x
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发表时间：
2008-11-01
影响因子：
3.1
通讯作者：
Chakrabarti, Abhijit
中科院分区：
文献类型：
--
作者：
Banerjee, Debasis;Saha, Sutapa;Chakrabarti, Abhijit
透射电镜研究发现，在一个新的溶血性贫血病例中，红细胞鬼膜上有大孔，细胞骨架破坏，循环红细胞微胞增多。与正常红细胞相比，年轻红细胞中磷脂酰丝氨酸（PS）不对称性的损失更大。唾液化糖缀合物的水平，如糖蛋白，通过小麦胚芽凝集素的结合来测量，在衰老过程中显示出更大的损失。PS不对称的剧烈丧失导致更快的吞噬，这是由含糖蛋白的微泡脱落介导的，使高度暴露于PS的红细胞能够被吞噬细胞接触。
Transmission electron microscopic study revealed large pores on the erythrocyte ghost membranes, disrupted cytoskeleton and microcytosis of circulating erythrocytes in a novel case of hemolytic anemia. Greater loss of phosphatidylserine (PS) asymmetry was observed in younger erythrocytes compared with the aged ones in contrast to the normal red cells. Levels of sialylated glycoconjugates, such as glycophorin, measured by the binding of wheat germ agglutinin, showed greater loss upon aging. Such drastic loss of PS asymmetry leads to faster eryptosis, mediated by shedding of glycophorin-containing microvesicles leaving highly PS-exposed erythrocytes accessible to the phagocytes.