Dalal Seema, Klemba Michael
Department of Biochemistry, Virginia Tech, Blacksburg, VA 24061, USA.
Department of Biochemistry, Virginia Tech, Blacksburg, VA 24061, USA.
Mol Biochem Parasitol. 2015 Jun;201(2):116-22. doi: 10.1016/j.molbiopara.2015.07.002. Epub 2015 Jul 26.
The endocytosis and catabolism of large quantities of host cell hemoglobin is a hallmark of the intraerythrocytic asexual stage of the human malaria parasite Plasmodium falciparum. It is known that the parasite's production of amino acids from hemoglobin far exceeds its metabolic needs. Here, we show that P. falciparum effluxes large quantities of certain non-polar (Ala, Leu, Val, Pro, Phe, Gly) and polar (Ser, Thr, His) amino acids to the external medium. That these amino acids originate from hemoglobin catabolism is indicated by the strong correlation between individual amino acid efflux rates and their abundances in hemoglobin, and the ability of the food vacuole falcipain inhibitor E-64d to greatly suppress efflux rates. We then developed a rapid, sensitive and precise method for quantifying flux through the hemoglobin endocytic-catabolic pathway that is based on leucine efflux. Optimization of the method involved the generation of a novel amino acid-restricted RPMI formulation as well as the validation of D-norvaline as an internal standard. The utility of this method was demonstrated by characterizing the effects of the phosphatidylinositol-3-kinase inhibitors wortmannin and dihydroartemisinin on the kinetics of Leu efflux. Both compounds rapidly inhibited Leu efflux, which is consistent with a role for phosphtidylinositol-3-phosphate production in the delivery of hemoglobin to the food vacuole; however, wortmannin inhibition was transient, which was likely due to the instability of this compound in culture medium. The simplicity, convenience and non-invasive nature of the Leu efflux assay described here makes it ideal for characterizing the in vivo kinetics of hemoglobin endocytosis and catabolism, for inhibitor target validation studies, and for medium-throughput screens to identify novel inhibitors of cytostomal endocytosis.
大量吞噬和分解宿主细胞血红蛋白是人类疟原虫恶性疟原虫红细胞内无性阶段的一个标志。已知该寄生虫从血红蛋白中产生氨基酸的量远远超过其代谢需求。在此,我们表明恶性疟原虫会将大量特定的非极性(丙氨酸、亮氨酸、缬氨酸、脯氨酸、苯丙氨酸、甘氨酸)和极性(丝氨酸、苏氨酸、组氨酸)氨基酸外排到细胞外培养基中。单个氨基酸外排速率与其在血红蛋白中的丰度之间的强相关性,以及食物泡内组织蛋白酶抑制剂E - 64d极大抑制外排速率的能力,表明这些氨基酸源自血红蛋白分解代谢。然后,我们开发了一种基于亮氨酸外排的快速、灵敏且精确的方法,用于定量通过血红蛋白内吞 - 分解代谢途径的通量。该方法的优化涉及生成一种新型的氨基酸限制型RPMI配方,以及验证D - 正缬氨酸作为内标。通过表征磷脂酰肌醇 - 3 - 激酶抑制剂渥曼青霉素和双氢青蒿素对亮氨酸外排动力学的影响,证明了该方法的实用性。这两种化合物都迅速抑制亮氨酸外排,这与磷脂酰肌醇 - 3 - 磷酸生成在将血红蛋白递送至食物泡中的作用一致;然而,渥曼青霉素的抑制是短暂的,这可能是由于该化合物在培养基中不稳定所致。本文所述的亮氨酸外排测定法的简单性、便利性和非侵入性,使其非常适合用于表征血红蛋白内吞和分解代谢的体内动力学、抑制剂靶点验证研究,以及用于中等通量筛选以鉴定新的胞口内吞抑制剂。