Krogstad D J, Sutera S P, Marvel J S, Gluzman I Y, Boylan C W, Colca J R, Williamson J R, Schlesinger P H
Department of Medicine, Washington University, St. Louis, Missouri 63110.
Blood Cells. 1991;17(1):229-41; discussion 242-8.
In the studies reported here, we examined the role of calcium in the maturation of the human malaria parasite Plasmodium falciparum, and in the loss of red cell deformability associated with parasite maturation. P. falciparum alters the permeability of its host red cell, which normally maintains submicromolar cytoplasmic concentrations of calcium. Infection of the red cell and parasite maturation produce a 30-fold increase in calcium uptake. Both parasite maturation and the loss of red cell deformability are blocked by EGTA (by extracellular-free calcium concentrations less than or equal to 35 microM) and by other calcium antagonists. The loss of red cell deformability that occurs with parasite maturation is accompanied by alterations in the cytoskeletal proteins of parasitized red cells similar to those produced by the calcium ionophore A23187 (reductions in bands 2.1 [ankyrin], 4.1, and 5 [actin]). These results establish that parasite development and the loss of red cell deformability are calcium-dependent. They suggest that parasite-induced changes in the calcium permeability of the red cell activate endogenous transglutaminase activity by raising the free calcium concentration of the red cell cytoplasm.
在本文报道的研究中，我们研究了钙在人类疟原虫恶性疟原虫成熟过程中的作用，以及在与寄生虫成熟相关的红细胞变形性丧失中的作用。恶性疟原虫会改变其宿主红细胞的通透性，正常情况下红细胞胞质钙浓度维持在亚微摩尔水平。红细胞感染和寄生虫成熟会使钙摄取增加30倍。寄生虫成熟和红细胞变形性丧失均被乙二醇双四乙酸（EGTA，细胞外游离钙浓度小于或等于35微摩尔）以及其他钙拮抗剂所阻断。寄生虫成熟时发生的红细胞变形性丧失伴随着被寄生红细胞细胞骨架蛋白的改变，这与钙离子载体A23187所产生的改变相似（带2.1[锚蛋白]、带4.1和带5[肌动蛋白]减少）。这些结果表明，寄生虫发育和红细胞变形性丧失是依赖钙的。它们提示，寄生虫诱导的红细胞钙通透性变化通过提高红细胞胞质游离钙浓度激活内源性转谷氨酰胺酶活性。
