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首页> 外文期刊>Cellular Signalling >Calmidazolium evokes high calcium fluctuations in Plasmodium falciparum
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Calmidazolium evokes high calcium fluctuations in Plasmodium falciparum

机译：Calmidazolium引起恶性疟原虫的高钙波动

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摘要

Calcium and calmodulin (CaM) are important players in eukaryote cell signaling. In the present study, by using a knockin approach, we demonstrated the expression and localization of CaM in all erythrocytic stages of Plasmodium falciparum. Under extracellular Ca2+-free conditions, calmidazolium (CZ), a potent CaM inhibitor, promoted a transient cytosolic calcium ([Ca2+](cyt)) increase in isolated trophozoites, indicating that CZ mobilizes intracellular sources of calcium. In the same extracellular Ca2+-free conditions, the [Ca2+](cyt) rise elicited by CZ treatment was similar to 3.5 fold higher when the endoplasmic reticulum (ER) calcium store was previously depleted ruling out the mobilization of calcium from the ER by CZ. The effects of the Ca2+/H+ ionophore ionomycin (ION) and the Na+/H+ ionophore monensin (MON) suggest that the [Ca2+](cyt)-increasing effect of CZ is driven by the removal of Ca2+ from at least one Ca2+-CaM-related (CaMR) protein as well as by the mobilization of Ca2+ from intracellular acidic calcium stores. Moreover, we showed that the mitochondrion participates in the sequestration of the cytosolic Ca2+ elicited by CZ. Finally, the modulation of membrane Ca2+ channels by CZ and thapsigargin (THG) was demonstrated. The opened channels were blocked by the unspecific calcium channel blocker Co2+ but not by 2-APB (capacitative calcium entry inhibitor) or nifedipine (L-type Ca2+ channel inhibitor). Taken together, the results suggested that one CaMR protein is an important modulator of calcium signaling and homeostasis during the Plasmodium intraerythrocytic cell cycle, working as a relevant intracellular Ca2+ reservoir in the parasite. (C) 2015 Elsevier Inc. All rights reserved.
机译：钙和钙调蛋白（CaM）是真核细胞信号传导中的重要角色。在本研究中，通过使用敲入方法，我们证明了CaM在恶性疟原虫所有红细胞生成阶段的表达和定位。在无细胞外Ca2 +的条件下，有效的CaM抑制剂Calidazoazolium（CZ）促进了孤立滋养体中瞬时细胞质钙（[Ca2 +]（cyt））的增加，表明CZ动员了细胞内钙的来源。在相同的无细胞外Ca2 +的条件下，CZ处理引起的[Ca2 +]（cyt）升高大约是以前内质网（ER）钙存储的消耗量增加了3.5倍，从而排除了CZ从ER迁移钙的可能性。 。 Ca2 + / H +离子载体离子霉素（ION）和Na + / H +离子载体莫能菌素（MON）的作用表明CZ的[Ca2 +]（cyt）增强作用是由至少一种Ca2 + -CaM中的Ca2 +去除驱动的相关（CaMR）蛋白，以及从细胞内酸性钙存储中动员的Ca2 +。此外，我们表明线粒体参与了CZ诱导的胞质Ca2 +的螯合。最后，证明了CZ和毒胡萝卜素（THG）对膜Ca2 +通道的调节。开放的通道被非特异性钙通道阻滞剂Co2 +阻断，但未被2-APB（电容性钙进入抑制剂）或硝苯地平（L型Ca2 +通道抑制剂）阻断。两者合计，结果表明，一种CaMR蛋白是疟原虫内红细胞周期中钙信号和稳态的重要调节剂，在寄生虫中作为相关的细胞内Ca2 +贮藏库。 （C）2015 Elsevier Inc.保留所有权利。

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